
Qass 
Book 



COPYRIGHT DEPOSIT 



A HANDBOOK OF 

PATHOLOGICAL ANATOMY 



HISTOLOGY Zili 

With an Introductory Section on 

POST-MORTEM EXAMINATIONS AND THE METHODS OF 
PRESERVING AND EXAMINING DISEASED TISSUES 



FRANCIS DELAFIELD, M.D., LL.D. 

Professor of the Practice of Medicine, College of Physicians and Surgeons, 
Columbia University, New York 



T. MITCHELL PRUDDEN, M.D., LL.D. 

Professor of Pathology and Director of the Department of Pathology, College of 
Physicians and Surgeons, Columbia University, New York 



Stxtb leMtion 

WITH 13 FULL-PAGE PLATES AND 453 ILLUSTRATIONS IN THE TEXT 
IN BLACK AND COLORS 






NEW YORK 

WILLIAM WOOD AND COMPANY 

MDCCCCI. 



THE LIBRARY OF 
CONGRESS, 

Two Copies Recewed 

SEP. U 1901 

iOPYRIQHT ENTRY 

CLASS A/XXc N» 
COPY B. 




Copyright, 1901 
By WILLIAM WOOD AND COMPANY 



THE PUBLISHERS' PRINTING COMPANY 
NEW YORK 






% 



'\ 



PREFACE 

TO THE SIXTH EDITIOX. 



It has been the iutention in the preparation of this, as in former edi- 
tions of this work, to give to students and practitioners of medicine, first, 
the knowledge necessary for the making of autopsies, the preservation 
of tissues and their preparation for microscopic study, and to outline the 
characters and methods of study of pathogenic micro- organisms; second, 
to describe concisely, with such illustrations as seem necessary, the le- 
sions of the acute infectious diseases, and so far as they are known, the 
micro-organisms inciting them ; the various iDhases of degeneration and 
inflammation ; the character of tumors ; the lesions of the general dis- 
eases, of j)oisoning, and of violent deaths ; and finally, to describe briefly 
the special lesions of different tissues and organs of the body. 

AMiile the general aims of the book have remained unchanged, it has 
seemed wise in this, more than in the earlier editions, to call attention 
here and there to the relationships of pathology to the allied phases of 
biological science, and where it might be done without hazard of the 
more urgent practical aims of the work to link the knowledge of disease 
and its lesions to the doctrines of evolution, and to view pathology as 
one aspect of the diverse manifestations of life and of energy, rather 
than as belonging to a special and exclusively human domain. 

Dr. Delafield has retired from an active share in the preparation of 
this edition ; so that the writer, deprived to his great regret of the wise 
counsel and large experience of the senior author, is alone responsible 
for such alterations and additions as have been made in this revision. 

The references in foot-notes have been considerably increased. The 
intention in this has been in part to indicate special studies or reviews 
relating to the theme under consideration; but more particularly to 
point out here and there publications in which a fuller bibliography may 
be found than is consistent with the scope and limitations of this work. 

The sections on the blood which were rewritten for the last edition 
by Dr. James Ewing have been revised for this, in such measure as the 
growth of knowledge seems to require, by Dr. Francis C. Wood. Dr. 
Wood has also written for this edition an entirely new section on malaria. 

The chapter on the nervous system has been revised, and in part, es- 
pecially the sections on normal morphology, degeneration, and inflam- 
mation, entirely rewritten by Dr. Frederick E. Bailey. To Drs. Wood 
and Bailey, as well as to Dr. Eugene Hodenpyl, Dr. Philip Hanson 
Hiss, Jr., Dr. John H. Larkin, and Dr. Augustus Jerome Lartigau, also 



IV PREFACE TO THE SIXTH EDITION. 

my colleagues, I am under great obligation for aid and for many helpful 
suggestions in various parts of this revision. 

The excellence of the many new photographs which have been repro- 
duced in the plates and in the text is due to the skill of Dr. Edward 
Leaming to whom I am much indebted. 

The work has been revised throughout. Many sections have been 
wholly rewritten, and a large number of new illustrations have been 
added to supplement or replace the old. The new colored plate illustrat- 
ing the Plasmodium malarise was drawn by Dr. Wood ; that illustrating 
lesions of ganglion cells, by Dr. Bailey. 

T. Mitchell Prudden. 



CONTENTS. 



PAET FIRST. 

THE METHOD OF MAKING POST-MOETEM EX AMI:N^ ATIONS ; 
THE LESIONS m CERTAIN FORMS OF DEATH FROM VIO- 
LENCE AND SUDDEN DEATH ; AND THE METHODS OF 
PRESERVING AND EXAMINING PATHOLOGICAL TISSUES. 

CHAPTER I. 

The Method of Making Post-Mortem Examinations, 3. — General considerations, 
3. — External inspection, 4. — Internal examination, 8. — The head, 9. — The spinal 
cord, 17. — The thorax and abdomen, 19. — The closure of the body, 36. — Bacterial 
examination of post-mortem specimens, 37. — Autopsies in medico-legal cases, 37. — 
Autopsies in cases of suspected poisoning, 38. — Examination of bodies of new-born 
children, 39. 

CHAPTER II. 

The Lesions in Certain Forms of Death from Violence; Sudden Death, 44. 
— Suffocation; Asphyxia, 44. — Death from strangulation; Hanging, 45. — Death 
from drowning, 46. — Death from electricity, 48. — Death from burning; Sudden 
death, 49. 

CHAPTER III. 

General Methods of Preserving Pathological Specimens and Preparing 
Them for Study, 51. — The study of fresh tissues; Rapid fixation and frozen sec- 
tions, 51. — Fixation, hardening, and preservation, 52. — Decalcif3ing; embedding 
and section cutting, 55. — Methods of staining, 59. — Methods of preserving speci- 
mens for gross demonstration and for museums, 61. — The importance of careful 
fixation and preservation, 61. 

PAET SECOISTD. 

GENERAL PATHOLOGY. 

Introduction, 65. 

CHAPTER I. 

Changes in the Circulation of the Blood; Hypera^mia and anaemia; Haemor- 
rhage and transudation, 69. — Thrombosis and embolism, 72. 

CHAPTER II. 

Atrophy, Degeneration, Pigmentation, and Necrosis. 78. — General considera- 
tions; atrophy, 78. — Degeneration, 79. — Pigmentation, 87. — Necrosis, 89. 

CHAPTER III. 

Hypertrophy, Hyperplasia, Metaplasia, Regeneration, 93. — Hypertrophy and 
hyperplasia, 93. — Regeneration, 94. — Modes of cell division, 95. — Regeneration of 
special tissues, 99. 



VI CONTENTS. 



CHAPTER IV. 



Inflammation, 107. — General Considerations, 107. — Types of inflammatory reaction 
of tlie body to injury, 108. — The healing of wounds. 111. — Hyperplasia and inter- 
stitial inflammation, 121. — Special phases of inflammation, 122. — Survey of the in- 
flammatory process and its significance, 123. 

CHAPTER V. 
Animal Parasites, 128. ^Protozoa, 128. — Worms, 130. — Arthropods, 139. 

CHAPTER VI. 

Plant Parasites, 140. — Bacteria, 140. — Methods of study of bacteria, 149. — Yeasts, 
156.— Moulds, 156. 

CHAPTER VII. 

The Relations of Micro-organisms to Disease; Infection and Immunity, 159. — 
The occurrence of bacteria and other micro-organisms in the body; its protective 
mechanism, 159. — Action of bacteria and their products in the body, 160. — Proofs 
of infective nature of bacteria found in the body, 162. — Conditions influencing the 
occurrence of infectious diseases, 163. — Infection and immunity, 164. 

CHAPTER VIII. 

The Infectious Diseases, 174. — General considerations, 174. — Suppurative and allied 
forms of inflammation, 175. — Toxaemia, 178. — Septicaemia and pyaemia, 179. — The 
pyogenic bacteria, 181. — Erysipelas, 185. — Infectious pseudo-membranous inflam- 
mation of mucous membranes, 186. — Other bacteria which are frequent excitants 
of suppuration, 187. — Acute lobar pneumonia and other infectious diseases induced 
by the Micrococcus lanceolatus, 190. — Gonorrhoea and other inflammatory lesions 
induced by the Micrococcus gonorrhoeae, 192. — Acute cerebro-spinal meningitis, 194. 
— Glanders, 195. — Anthrax, 197. — Actinomycosis, 199. — Other organisms resembling 
actinomyces, 201. — Influenza, 202. — Typhoid fever, 203. — Asiatic cholera, 214. — 
Tuberculosis, 217. — Bacteria resembling the tubercle bacillus, 229. — Lepra, 230. — 
Syphilis, 232.— Diphtheria, 235.— Tetanus, 239.— Relapsing fever, 241.— Malta 
fever, 241. — Bubonic plague, 242. — Haemorrhagic septicaemia, 243. — Hydrophobia, 
245.— Typhus fever, 247.— Yellow fever, 248.— Variola, 249.— Scarlet fever, 250.— 
Measles; whooping-cough; beri-beri, 251. — Acute rheumatism, 252. — Malaria, 252. 
— The infectious diseases of animals, 260. — Bibliography of the infectious diseases, 
260. 

CHAPTER IX. 

Tumors, 261. ^The nature and characters of tumors in general, 261. — The etiology of 
tumors, 267. — Classification of tumors, 274. — Tumors formed by various combina- 
tions of tissue types, 275. — Complex congenital growths, teratoma, 276. — Special 
tumor types, 270. — Cysts, 277. — Special forms of tumors, 279. — Bibliography of 
tumors, 319. 

CHAPTER X. 

The Lesions Induced by Poisons, 320. — Forms of poisons, 320.— The lesions induced 
by exogenous poisons, 321. — Lesions induced by endogenous poisons, autointoxica- 
tions, 328. 

CHAPTER XI. 

General Diseases, 331. — Cachexia strumipriva, myxoedema, 331. — Exophthalmic 
goitre; Addison's disease, 332. — Diabetes mellitus, 333 — Gout; sunstroke, 335. — 
Scorbutus, 336. — Acromegalia, 336. — Purpura, 337. — Lymphatic constitution, 337, 



CONTENTS. vii 



PART THIRD. 

SPECIAL PATHOLOGY. 

General Considerations, 341. 

CHAPTER I. 

The Blood and the Blood-forming Organs, 342. — Changes in the compositiou and 
structui'e of the blood, 342. — Alterations in the red blood cells, 343. — Alterations in 
the white blood cells, 347. — Methods of examination of the blood, 352. — Foreign 
bodies in the blood, 353. — General diseases involving the blood and blood-forming 
organs; chlorosis, 355. — Secondary anaemia, 356. — Pernicious angemia, 356. — Leu- 
kaemia, 358. — Pseudoleuka^mia, 360. — Anaemia infantum pseudo-leukaemica, 361. 

CHAPTER II. 

The Lymph-Nodes, 362. — General characteristics of the lymph-nodes ; atrophy, 362. — 
Degeneration; pigmentation, 363. — Inflammation, 364. — Hyperplasia of the lymph- 
nodes, 369. — Tumors; parasites, 370. 

CHAPTER HI. 

The Spleen and Thymus, 371. — General characteristics of the spleen, malformations 
and displacements, 371. — Wounds, ruptures, and haemorrhage ; atrophy; degenera- 
tion, 372. — Pigmentation; disturbances of the circulation, 373. — Inflammation, 375. 
— Chronic endothelial hyperplasia, 379. — Alterations in leukaemia and pseudo-leu- 
kaemia; tumors; parasites, 380. — The thymus, 381. — Malformation and hyper- 
trophy; haemorrhage; inflammation; tumors, 381. . 

CHAPTER IV. 

The Thyroid and Adrenals, 382. — The Thyroid: Malformations; degeneration, 382. 
— Disturbances of circulation; inflammation; struma, 383. — Tumors, 384. — Para- 
sites, 385. — Ihe Adrenals, 385. — Malformations; atrophy and degeneration; throm- 
bosis and haemorrhage ; inflammation, 385. — Tumors, 386. 

CHAPTER V. 

The Circulatory System, 387. — The Pericardium, 387. — Injuries; haemorrhage; 
dropsy; pneumonotosis, 387. — Inflammation, 388. — Tumors, 390.— The Heart, 390. 
— Malformations and malpositions, 390. — Wounds and ruptures, 393. — Atrophy, 
394. — Hypertrophy, 395. — Dilatation: changes in the valves, 396. — Aneurism, 397. 
— Thrombosis, 398. — Degeneration, 400. — Segmentation and fragmentation of the 
myocardium, 402. — Thrombosis and embolism of the coronary arteries, 402. — In- 
flammation, 403. — Tumors, 410. — Parasites, 410. — The Blood- Vessels, 410. — Atrophy 
and hypertrophy, 410. — The Arteries: Rupture and wounds, 410. — Degeneration, 
411. — Inflammation, 412. — Aneurism, 418. — Aneurism of the different arteries, 420. 
— Stenosis and obliteration of the aorta, 421. — Tumors, 421. — The Veins: Dilata- 
tion, 422. — Wounds and rupture; thrombosis; degeneration; inflammation, 423. — 
Tumors; parasites, 425. — The Capillaries, 425. — T he Lyniph- Vessels : General char- 
acteristics; lymphangiectasis ; inflammation, 426. — Tumors, 427. 

CHAPTER YI. 

The Respiratory System, 429. — The Nose and Associated Cavities: Inflammation; 
tumors, 429. — The Larynx and Trachea: Malformations; oedema of the glottis; in- 
flammation, 430. — Tumors, 432. — The Pleura: Hydrothorax; hy dropneumo thorax ; 
P3^opneumothorax ; haemorrhage; inflammation, 433. — Tumors, 437. — The Bronchi: 



Vlil CONTENTS. 

Haemorrhage; inflammation, 438. — Bronchiectasia, 441, — Tumors, 442. — Lesions 
of the tracheal and bronchial lymph-nodes, 442. — The Lungs: Malformations; in- 
juries; perforations; disturbances of circulation, 443. — Haemorrhage and infarction, 
445. — Atelectasis, 446. — Emphysema, 447. — Gangrene, 448.— Inflammation, 449. — 
Tuberculous pneumonia, 462. — Tumors, 480. — The mediastinum, 481. 

CHAPTER YH. 

The Digestive System, 482. — The Mouth: Malformations; inflammation, 482. — 
Tumors, 484. — The Tongue: Malformations, 484. — Hypertrophy and inflammation; 
tumors; micro-organisms, 485. — The Pharynx : Malformations, 486. — Inflammation 
487. — Tumors, 489. — The CEsophagus : Malformations; perforation and rupture; 
haemorrhage; dilatation, 490. — Stenosis, 491. — Inflammation; tumors, 492. — The 
Stomach : Malformations; cadaveric changes; injuries, 493. — Haemorrhage; atrophy 
and degeneration, 494. — Inflammation, 495. — Ulcers, 498. — Dilatation; tumors, 500. 
— Foreign bodies, 503. — The Intestines: Malformations, 503. — Incarceration, 504. 
— Intussusception; dilatation; wounds and ruptures, 505. — Disturbances of circu- 
lation; haemorrhage; degeneration; inflammation, 506. — Tumors, 518. — Concre- 
tions, 520. — T he Peritoneum : Malformations; ascites; inflammation, 521. — Tumors, 
524. — Cysts; parasites, 526. — The Salivary Glands: Inflammation, 526. — Tumors, 
528. — The Pancreas: Malformations; displacements; atroph}^; degeneration; ne- 
crosis, 529. — Tumors, 532. — Concretions; foreign bodies, 533. 

CHAPTER VIII. 

The Liver, 534. — Malformations; changes in size and position, 534. — Wounds; rup- 
ture; hgemorrhage; anaemia; hyperaemia, 535. — Lesions of the hepatic vessels, 537. 
— Atrophy; degeneration, 539. — Pigmentation, 543. — Calcification; inflammation, 
544. — Hyperplasia of lymphatic tissue; tumors, 554. — Parasites, 557. — Lesions of 
the biliary passages and the gall ducts, 559. — Tumors of the gall bladder and ducts, 
561. — Biliary calculi, 562. 

CHAPTER IX. 

The Urinary Organs, 564. — The Kidneys: Malformations; changes in position; com- 
pensatory In'pertrophy, 564. — Disturbances of circulation, 565. — Albuminuria and 
casts, 566. — Degeneration, 567. — Inflammation, 570. — Suppurative pyelitis and 
pyelo-nephritis, 587.— Hydronephrosis; perinephritic suppuration, 588. — Cysts, 
589. — Renal calculi; tumors, 590. — Parasites, 592. — The Urinary Bladder: Mal- 
formations, 592. — Changes in size and position, 593. — Wounds; rupture; perfora- 
tion, 594. — Disturbances of circulation; inflammation, 595. — Tumors, 597. — Para- 
sites; foreign bodies; calculi, 598. — The Urethra: Malformations; changes in size 
and position, 599. — Wounds; rupture; perforation; inflammation, 600. — Tumors, 
601. 

CHAPTER X. 

The Reproductive Organs op^ the Female, 602. — The Vulva: Malformations; 
haemorrhage; hyperaemia; inflammation, 602. — Tumors, 603. — The Vagina: Mal- 
formations; changes in size and position, 604. — Wounds; perforations; inflamma- 
tion, 605. — Tumors; parasites, 606. — The Uterus: Malformations, 606. — Changes 
in size, 607. — Changes in position, 608. — Rupture; perforation; hyperaemia; 
haemorrhage, 609. — Atrophy and degeneration, 610. — Inflammation, 611. — Tumors, 
616. — Parasites and cysts, 626. — Placenta: Degeneration; haemorrhage; inflamma- 
tion, 627. — Tumors, 628. — The Ovaries: Malformations; changes in size and posi- 
tion, 628. — Hyperaemia and haemorrhage; inflammation, 629. — Tumors, Q'^l.—The 
Fallopian Tubes : Malformations ; changes in size and position ; haemorrhage, 638. 
— Inflammation; tumors, 639. — Extra-uterine pregnancy, 640. — The Mamma: Mal- 
formations; haemorrhage; inflammation, 641. — Tumors, 643. 



CONTENTS. ix 



CHAPTER XI. 



Reproductive Organs of the Male, 649. — The Penis: Malformations, 649. — Injury; 
liaemorrbage ; inflammation; tumors, (550..— The Scrotirm : Tumors, 651. — I'he Tes- 
ticles: Malformations, 651. — Hydrocele, 652. — Hiematocele; spermatocele; atrophy; 
inflammation, 653. — Tumors, 656. — Parasites, 657. — The Seminal Fmcfes .• Tumors, 
657. — The Prostate: Degeneration; atrophy; hypertrophy, 657. — Inflammation, 
658. — Tumors; parasites; concretions, 659. — CoiDper's Glands, 659. — The male 
mamma, 660. 

CHAPTER XII. 

The Bones and Joints, 661. — The Bones: Atrophy; disturbances of circulation, 661. 
— Healing of wounds and fractures, 662. — Inflammation, 663. — Necrosis, 672. — 
Caries, 673. — Rachitis, 674. — Osteomalacia, 677. — Alterations in bone marrow in 
leukaemia and anaemia, 677. — Tumors, 678. — The Joints: Degeneration; inflamma- 
tion, 682.— Tumors, 685. 

CHAPTER XIII. 

'Voluntary Muscle, 687. — Necrosis; atrophy; hypertrophy, 687. — Degeneration, 690. 
— Injuries; haemorrhage; infarction, 691. — Inflammation, 692. — Tumors, 693. — 
Parasites, 694. 

CHAPTER XIV. 

The Nervous System, 695. — The Dura Mater Cerehralis : Haemorrhage; thrombosis, 
695. — Inflammation, 696. — Tumors, 698. — The Pia Mater Cerehralis: General con- 
siderations, 699.— CEdema; hyperaemia and haemorrhage, 700. — Inflammation, 701. 
— Tumors, 706. — Parasites, 708. — Dura Mater Spinalis: Ha3morrhage; inflamma- 
tion; tumors; parasites, 709. — Pia Mater Spinalis: Haemorrhage; inflammation; 
tumors ; parasites, 710. — The Ventricles of the Brain, the Ependyma and Choroid 
Plexus: General considerations; inflammation, 711. — Tumors; parasites, 714 — The 
Brain: Malformations, 714. — The Spinal Cord : Malformations, 715. — In juries of the 
brain, 717. — Injuries of the cord; injuries of the nerves, 718. — Hypertrophy and 
atrophy of the brain, 719. — Pigmentation of the brain, 720. — Circulatory and Vascular 
- Changes in the Brain and Spinal Cord : flyperaemia, 721. — (Edema ; haemorrhage, 722. 
— Thrombosis and embolism, 727. — Lesions of the vessel walls in the brain and cord, 
730. — Degeneration and Inflammation of the Brain, Spinal Cord, and Nerves, 730. 
— Review of normal morphology, 730. — Degeneration : Neurone degeneration,~735. 
— Regeneration, 739. — Degeneration affecting systems of neurones, 740. — hiflamma- 
tion, 751. — Lesions of the brain in general paresis of the insane, 759. — Tuberculous 
lesions of the nervous system, 762.— Syphihtic lesions of the nervous system, 763. — 
Actinomycosis; leprosy; tumors, 764. — Parasites, 767. — Holes and cysts, 767. — 
Pineal gland, 768. — Hypophysis cerebri, 768. — Methods of preparation of nerve 
tissue for microscopic study, 769. 



LIST OF ILLUSTEATIONS. 



FIG. 
1. 

2. 
3. 

4. 

5. 
6. 

7. 



10. 
11. 
12. 
13. 
14. 
15. 
16. 
17. 
18. 
19. 
20. 
21. 
22. 
23. 
24. 
25. 
26. 
27. 
28. 
29. 
30. 
31. 
32. 
33. 
34. 
35. 
36. 
37. 
38. 
39. 
40. 
41. 
42. 
43. 
44. 
45. 
46. 



Side view of the human brain, showing its fissures and convolutions, 

Method of opening the brain, first incisions, 

Method of opening the brain, final incisions, 

View of the base of the brain, with the temporal lobes turned backwar 

outward, — Meynert's method, 
Drawing of the brain axis, separated from the brain mantle, 
Brain mantle, seen from below. 
Outlines of spinal-cord sections, 
Occluding thrombus of the iliac, 
Portion of red thrombus, . 
Lamellated thrombus. 
Organized thrombus. 
An embolus lodged at division of artery, 
Fat emboli in the lung. 
Infarctions of the spleen, . 
Albuminous degeneration — kidney, 
Fatty degeneration — kidney, 
Fatty infiltration of liver cells, . 
Amyloid degeneration of capillaries. 
Corpora amylacea. 
Glycogen infiltration, 
Serous infiltration, 
Mucous degeneration. 
Mucous degeneration of fibrous tissue. 
Hyaline degeneration. 
Pigmentation of lungs, 
Necrosis of epithelium — kidney, 
Coagulation necrosis in cells. 
Caseation in tubercle. 
Phases of mitosis, 
Abnormal phases of mitosis. 
Regeneration of striated muscle. 
Regeneration of epithelium, 
Regeneration of connective tissue, 
Development of blood-vessels, . 
Emigration of leucoc3"tes. 
Exudative inflammation in appendix. 
Fibrin in inflammatory exudate, 
Fibrin forming around dead cells. 
Bacterial embolus in liver, 
Bacterial embolus in liver with necrosis, 
Necrosis and suppuration in liver, 
Phagocytes, .... 
Giant cells, .... 

Necrotic muscle ; absorption by phagocytes, 
Granulation tissue, 
Granulation tissue. 



d and 



PAGE 

, 11 
, 12 

13 

14 
15 
15 

18 
72 
73 

74 
74 
75 
75 
76 
79 
81 
81 
82 
83 
84 
84 
84 
85 



91 
91 
96 

97 
100 
101 
103 
104 
110 
110 
112 
112 
113 
113 
114 
116 
116 
117 
117 
118 



Xll 



LIST OF ILLUSTRATIONS. 



FIG. 

47. 
48. 
49. 
50. 
51. 
52. 
53. 
54. 
55. 
56 
57. 
58. 
59. 
60. 
61. 
62. 
63. 
64. 
65. 
66. 
67. 
68. 
69. 
70. 
71. 
■72. 
73. 
74. 
75. 
76. 
77. 
78. 
79. 
80. 
81. 
82. 
83. 
84. 
85. 
86. 
87. 
88. 
89. 
90. 
91. 
92. 
93. 
94. 
95. 
96. 
97. 



100. 
101. 
102. 



Fibroblasts, .... 

Healing wound in tongue of dog, 

Cicatricial tissue, 

Exuberent granulations, 

Amoeba coli, 

Coccidium oviforme, . 

Balantidium coli, 

Cercomouas intestinalis, 

Trichomonas vaginalis, 

Distoma liepaticum, ., 

Head of Taenia solium. 

Head and proglottides of Tsenia mediocanellata 

Cuticula of echinococcus cyst, 

Scolices of Taenia echinococcus, 

Hooklets from scolex of Taenia echinococcus, 

Ascaris lumbricoides, 

Eggs of nematode worms, . 

Oxyuris vermicularis, 

Trichocephalus dispar. 

Trichinae encysted in muscle 

Filaria sanguinis hominis, . 

Sarcoptes hominis, 

Pediculis capitis. 

Drawing of three typical forms of bacteria 

Bacilli showing tiagella, 

Bacteria with capsule. 

Growth aggregates of bacteria, . 

Sarcina, 

Bacilli showing spores, . . 
A Petri gelatin-plate culture, 
Colonies in plate culture, . 
Tube cultures, . . 
Tube culture — potato, . . . 

Tube culture showing gas formation, 
Petri plate culture from mouth, 
Cotton swab for collecting, 

Yeast, 

Aspergillus glaucus 

Achorion Schonleinii, 

Pus cells, 

Staphylococcus pyogenes aureus in cells, 

Focal necrosis in liver, 

Pyaemic pleurisy, .... 

Staphj^lococcus pyogenes aureus. 

Micrococci in abscess of kidney, 

Streptococcus pyogenes. 

Erysipelas of skin, .... 

Pseudomembranous inflammation, 

Diplococcus lanceolatus. 

Micrococcus gonorrhoeae in cells. 

Micrococcus gonorrhoeae in cultures, . 

Bacillus mallei, ..... 

Anthrax of the skin, .... 

Bacillus anthracis in liver, 

Bacillus anthracis containing spores, 

Actinomyces, . . . . 



PAGE 

. 119 
, 119 
, 120 
. 121 
. 128 
. 129 
. 130 
. 130 
. 130 
. 131 
. 131 
. 132 
. 132 
. 133 
. 133 
. 135 
. 135 
. 135 
. 136 
. 137 
. 138 
. 139 
. 139 
. 140 
. 141 
. 141 
. 142 
. 142 
. 143 
. 152 
. 152 
. 153 
; 153 
. 154 
. 155 
. 155 
. 156 
. 157 
. 157 
. 177 
. 177 
. 179 
. 180 
. 182 
. 182 
. 184 
. 185 
. 186 
.191 
. 193 
. 193 
. 196 
. 197 
. 198 
. 199 
, 200 



LIST OF ILLUSTRATIONS. 



Xlll 



FIG. 

103. Bacillus typhosus, 

104. Peyer's patch in typhoid fever, 

105. Ulcers of Peyer's patch in typhoid fever, . 

106. Ulcers of Peyer's patch in typhoid fever, . 

107. Endothelial-cell hyperplasia in typhoid fever, 

108. Focus of cell proliferation in liver — typhoid fever, 

109. H3q3erplasia of endothelium in liver — typhoid fever. 

110. Typhoid bacilli in spleen, . 

111. Spirillum cholera; Asiaticae, 

112. A miliary tubercle, 

113. A miliary tubercle, 

114. A miliary tubercle, 

115. Tuberculosis — exudative form, . 

116. Tubercle bacilli in sputum, 

117. Tubercle bacillus — man: culture, 

118. Tubercle bacillus — bird : culture 

119. Lesion of dead tubercle bacilli 

120. Lupus, 

121. Bacillus leprae, . 

122. Syphilitic inflammation, 

123. Syphilitic inflammation, 

124. Syphilitic inflammation, 

125. Syphilitic inflammation — gumma, 

126. Syphilitic inflammation — gumma, 

127. Fibrin in diphtheritic membrane, 

128. Diphtheritic inflammation 

129. Bacillus diphtheriae, . 

130. Bacillus tetanei, 

131. Spirocha^te Obermeieri, 

132. Hydrophobia, 

133. Variola, 

Plate. I. Haematozoa of Malaria, 
134; Cell "inclusions" in carcinoma, 

135. Dermoid cyst, 

136. Fibroma durum, 

137. Fibroma moUe, . 

138. Papilloma of skin, 

139. Mucous polyp of nose, 

140. Myxoma, . 

141. Sarcoma — spindle-celled, 

142. Sarcoma — spindle-celled, 

143. Sarcoma — round-celled, 

144. Sarcoma — round-celled, 

145. Melanosarcoma, . 

146. Giant-celled sarcoma, 

147. Angiosarcoma, . 

148. Angiosarcoma, . 



149. 
150. 
151. 
152. 
153. 
154. 
155. 
156. 
157. 



Angiosarcoma, 
Angiosarcoma, 
Myxosarcoma, 
Adenosarcoma, 
Endothelioma, 
Endothelioma, 
Endothelioma, 
Endothelioma, 
Endothelioma, 



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XIV 



LIST OF ILLUSTRATIONS. 



FIG. 

158. Endothelioma, 

159. Chondroma, 

160. Glioma, 

161 . Neuroglia cells, . 

162. Myoma, 

163. Fibro- myoma 

164. Neuroma, . 

165. False neuroma, . 

166. Multiple fibroma of nerves, 

167. Multiple fibroma of nerves, 

168. Angioma, .... 

169. Angioma, .... 

170. Lymphangioma, 

171. Carcinoma molle, 

172. Adenoma of mamma, 

173. Adenoma of stomach, 

174. Carcinoma of hand, 

175. Cancer cells in the tissue, . 

176. Cancer cells in a lymph-vessel, 

177. Metastatic carcinoma, 

178. Metastatic carcinoma, 

179. Inflammation in carcinoma, 

180. Epithelioma of neck, . 

181. Epithelioma of lymph-node, 

182. Epithelioma of skin, . 

183. Epithelioma of skin, . 

184. Epithelioma of hand, 

185. Congenital naevus of skin, . 

186. Epithelioma of nose, . 

187. Epithelioma of face, . 

188. Epithelioma of face, . 

189. Fibro-carcinoma, 

190. Carcinoma gelatinosum, 

191. Carcinoma myxomatodes, . 
Plate n. Blood. 

192. Pigmentation of bronchial lymph-node, 

193. iVcute inflammation of lymph-node, . 

194. Endothelial cells in hyperplasia of lymph-node 

195. Hyperplasia of Peyer's patch in typhoid fevei-, 

196. Chronic inflammation of lymph-node 

197. Amyloid degeneration of spleen, 

198. Hypersemia of spleen, 

199. Chronic indurative splenitis, 

200. Chronic interstitial splenitis, 

201. Malarial spleen, . 

202. Chronic endothelial hyperplasia of the spleen, 

203. Atrophied thyroid, 

204. Colloid struma, . 

205. Fibrinous pericarditis, 

206. Obliteration of pericardial sac 

207. Interventricular foramen — heart, 

208. Fenestration of semilunar valves, 

209. Atrophic pericardial fat, 

210. Aneurism of the heart, 

211. Polypoid thrombus in the heart. 

212. Globular thrombus in the right auricle 



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faces 346 

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. 399 



LIST OF ILLUSTRATIONS. 



XV 



FIG. 

213. Thrombus on mitral valve, 

214. Fatty degeneration of heart muscle, 

215. Fatty infiltration of heart muscle, 

216. Bacterial embolus in heart muscle, 

217. Chronic interstitial myocarditis, 

218. Ulcerative endocarditis, 

219. Chronic endocarditis, 

220. Vegetation on aortic valve, 

221. Chronic endocarditis, 

222. Chronic arteritis, 

223. Chronic arteritis, 

224. Connective tissue in arterio-sclerosis, 

225. Chronic arteritis, 

226. Chronic arteritis, 

227. Atheroma of the aorta, 

228. Atheroma of the aorta, 

229. Arteriosclerosis, .... 

230. Tuberculous arteritis, 

231. Aneurism of the arch of the aorta, 

232. Tuberculous phlebitis, 

233. Epithelial hyperplasia of vocal cords 

234. Endothelioma of pleura, 

235. Acute catarrhal bronchitis, 

236. Chronic bronchitis, 

237. Chronic fibrinous bronchitis, 

238. Adenoma of bronchi, . 

239. Tuberculous bronchial lymph-nodes, 
Plate III. Tuberculous Bronchial Lymph 

240. Chronic congestion of lung, 

241. Emphysema of lung, . 

242. Acute lobar pneumonia, 

243. Acute lobar pneumonia, 

244. Exudate in resolving pneumonia, 

245. Organizing pneumonia, 

246. Broncho-pneumonia in adult, 

247. Broncho-pneumonia in child, 

248. Broncho-pneumonic exudate, 

249. Broncho-pneumonia in child, 

250. Persistent broncho-pneumonia, . 

251. Broncho-pneumonia with streptococci, 

252. Chronic interstitial pneumonia, 

253. Chronic interstitial pneumonia, 

254. Anthracotic pigmentation of lung, 
Plate IV. Acute Miliary Tuberculosis of 

255. Miliary tubercle of lung, . 

256. Miliary tubercle of lung, . 

257. Miliary tubercle of lung, . 

258. Miliary tubercle of lung, . 

259. Fibrous tubercle, 
Plate V. Tuberculous Broncho -pneumonia 

260. Miliary tubercles and tuberculous broncho 
Plate VI. Tuberculous Broncho- pneumonia 

261. Tuberculous broncho-pneumonia, 
Plate VII. Pulmonary Tuberculosis . 

262. Tuberculous broncho-pneumonia, 

263. Tuberculous broncho-pneumonia, 



node 



the Lung 



pneumonia 



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faces 462 
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faces 466 
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faces 468 
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faces 470 
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XVI 



LIST OF ILLUSTRATIONS. 



FIG. 

264. Tuberculous broncho-pneumonia, 
Plate VIII. Chronic Pulmonary Tuberculosis, 

265. Fatty epithelium in chronic phthisis, 

266. Acute j)ulmonary tuberculosis, . 
Plate IX. Bronchiectatic Cavities in Pulmonary Tuberculosis, 

267. Chronic pulmonary tuberculosis, 
Plate X. Pulmonary Tuberculous Cavities, 
Plate XI. Chronic Pulmonary Tuberculosis, 

268. Experimental tuberculosis of lungs, . 

269. Experimental tuberculosis of lungs . 
Experimental tuberculosis of lungs, . 
Endothelioma of the lungs, 
Adenoma of the lungs, 

Plate XII. Chronic Pulmonary Tuberculosis, 
273. Carcinoma of the lung. 

Wall of branchial cyst of neck, . 

Wall of branchial cj^st of neck, . 

Adenoid polyp of pharynx, 

Fatt}^ degeneration of stomach, 

Acute catarrhal gastritis, . 



270. 
271. 

272. 



274. 

275. 
276. 
277. 
278. 

279. Chronic gastritis, . . . . 

280. Chronic gastritis, . . . . 

281. Chronic gastritis, . . . . 

282. Chronic ulcer of stomach, , 

283. Fibroma of stomach, .... 

284. Hair balls from human stomach, 

285. Diverticulum of small intestine, 

286. Multiple false diverticula of intestine, 

287. Acute catarrhal enteritis, . 

288. Nodular enteritis, .... 

289. Tuberculous ulcers of intestine, 

290. Tuberculous ulcer of intestine, . 

291. Subserous tubercles of intestine, 

292. Tuberculous ulcers of intestine, 

293. Acute catarrhal colitis, 

294. Amoebic colitis, 

295. Nodular colitis, 

296. Nodular colitis, 

297. Nodular colitis — ulcers, 

298. Necrotic colitis, 

299. Chronic colitis, 

300. Acute suppurative appendicitis, 

301. Lymphomata of the intestine, . , . 

302. Adenoma of the rectum, 

303. Acute cellular peritonitis, . 

304. Papilloma of the peritoneum, 

305. Cystic papilloma of the omentum, 

306. Endothelioma of the parotid, 

307. Fat necrosis in the pancreas, 

308. Chronic congestion of the liver, 

309. Chronic congestion of the liver, 

310. Fatty infiltration of liver cells, . 

311. Fatty infiltration of the liver, 

312. Amyloid degeneration of the liver, 

313. Malarial pigmentation of the liver, 
. 314. Small abscess of the liver, . 



faces 

faces 
faces 



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474 
475 
476 
478 
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LIST OF ILLUSTEATIOXS. 



XVU 



FIG. 

315. Cirrhosis of the liver, .... 

316. Cirrhosis of the liver, . . 

317. Cirrhosis of the iiver, .... 

318. Cirrhosis of the liver — neAV-formed gall-ducts, 

319. Hypertrophic cirrhosis of the liver, . 

320. Gumma of the liver, 

321. Carcinoma of the liver, .... 

322. " Foamy " liver, 

323. Echinococcus multil ocularis in liver, 

324. Suppurative inflammation of the gall-ducts, 

325. Adenoma of the gall-ducts, 

326. Hyaline globules in tubule of kidney, 

327. Hyaline casts in uriniferous tubule, . 

328. Albuminous degeneration of kidney, 

329. Fatty degeneration of epithelium in kidney, 

330. Amyloid degeneration of capillaries in kidney, 

331. Glycogen degeneration of epithelium in kidney 

332. Acute diffuse neiDhritis, 

333. Acute diffuse nephritis, 

334. Acute diffuse nephritis, 

335. Acute diffuse nephritis, 

336. Acute diffuse nephritis, 

337. Diffuse nephritis, persistent, 

338. Atrophied glomerulus of kidnej 

339. Chronic diffuse nephritis, . 

340. Chronic diffuse nephritis, . 

341. Chronic diffuse nephritis, . 

342. Chronic diffuse nephritis, . 

343. Chronic diffuse nephritis, . 

344. Chronic diffuse nephritis. . 

345. Obliterating endarteritis in chronic diffuse 

346. Tuberculous nephritis, 
347.' Chronic pyelo-nephritis, 

348. Congenital cystic kidney, . 

349. Adenoma of the kidney, 

350. Adenoma of the kidney, 

351. Adenoma of the kidney, 

352. Diverticula of the bladder, 

353. Papilloma of the bladder, . 

354. Chronic endometritis, 

355. Chronic endometritis, 

356. Chronic endometritis, 

357. Hyperplasia of the cervix uteri 

358. Uterine phlebitis, 

359. Uterine polyp, . 

360. Glandular myoma of the uterus, 

361. Adenoma of the uterus, 

362. Adenoma of the uterus, 

363. Adenoma of the uterus, 

364. Adenoma of the uterus, 

365. Adenoma of the uterus, 

366. Carcinoma of the uterus, . 

367. Carcinoma of the uterus, . 

368. Carcinoma of the uterus, . 

369. Fragment of decidua, 

370. Deciduoma malignum, 



nephritis 



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551 

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592 

594 

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612 

612 

613 

614 

616 

617 

619 

620 

620 

621 

621 

622 

623 

624 

625 

625 

626. 



XVlll 



LIST OF ILLUSTEATIONS. 



FIG. 

371. Chronic oophoritis, 

872. Chronic ooplioritis, 

373. Papilloma of the ovary, 

874. Sarcoma of the ovar}^ 

375. Endothelioma of the ovary, 

876. Cyst-adenoma of the ovary, 

377. Cyst-adenoma of the ovary, 

378. Cyst-adenoma of the ovary, 

379. Papillary cysts of omentum, 

380. Hydro-salpinx, . 

381. Suppurative mastitis, 

382. Chronic mastitis, 
883. Intracanalicular fibroma of the mamma, 

384. Intracanalicular fibroadenoma of the m 

385. Pericanalicular fibroma of the mamma, 
886. Adenoma of the mamma, . 

387. Cyst-adenoma of the mamma, 

388. Carcinoma of the mamma, 

389. Chronic orchitis, 

390. Chronic orchitis, 

891. Hypertrophy^ of the prostate, 

892. Adenoma of the prostate, . 

893. Callus after fracture, 

394. Ossifying periostitis, . 

395. Ossifying periostitis, . 
896. Rarefying osteitis, 

397. Condensing osteitis, . 

398. Tuberculous osteitis, . 
899. Necrosis of bone, 

400. Rachitic bone, 

401. Cranio tabes, 

402. Sarcoma of bone, 

403. Progressive muscular atrophy, 

404. Progressive muscular atrophy, 

405. Pseudo-hypertrophy of muscle, 

406. Hyaline degeneration of muscle 

407. Chronic interstitial myositis, 

408. Pachymeningitis, 

409. Brain sand, 

410. Psammoma of the dura mater, 

411. Acute exudative meningitis, 

412. Acute exudative meningitis, 

413. Acute exudative meningitis, 

414. Fatty degeneration of cells of the pia mater 

415. Miliary tubercle of the pia mater, 

416. Miliary tubercle of the ependyma 

417. Endothelioma of the cerebellum, 

418. Endothelioma of the pia mater, 

419. Bone plates in the pia mater spinalis, 

420. Acute ependymitis, . 

421. Congenital hydrocephalus in child, 

422. Hydromyelia, .... 

423. False heterotopia of the spinal cord, 

424. Atrophy of the brain, 

425. Diagram of circle of Willis, 

426. Cerebral apoplexy. 



PAGE 

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670 
673 
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676 
680 
688 
689 
690 
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693 
696 
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699 
702 
702 
703 
704 
705 
706 
707 
708 
711 
712 
713 
716 
717 
719 
721 
725 



LIST OF ILLUSTRATIONS. 



XIX 



Hiemorrhage iuto the spiual cord, 
Hsematomyelopore, . . . 
Degenerated brain tissue in embolic softening, 
Fatty degeneration in blood-vessels of brain, 
Neurone, 
Neurone, 



riG. 
427 
428 
429 
430 
431 
432 

433. Neuroglia cell, . 
Plate XIII. Ganglion Cells 

434. Neuroglia cell, . 

435. Neurone degeneration 

436. Neurone degeneration 

437. Secondary descending degeneration, 

438. Secondary ascending degeneration, 

439. Amyotrophic lateral sclerosis, . 

440. Tabes dorsalis, .... 

441. Tabes dorsalis, .... 

442. Tabes dorsalis, .... 

443. Combined sj^stem disease, . 

444. Degenerated tissue in acute myelitis, 

445. Poliomyelitis anterior, 

446. Anterior poliomyelitis, 

447. Landry's paralysis, 

448. Landrj^'s paralysis — blood-vessels, 

449. Landry's paralysis — blood-vessels, 

450. Multiple neuritis, 

451. Multiple sclerosis in the spinal cord, 

452. Solitary tubercle of the cerebellum, 

453. Syringomyelia, , . . = 



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PART I. 



THE METHOD OF MAKING POST-MOETEM EX AMI:N^ ATIONS ; 

—THE LESIONS IN CEETAIN FOEMS OF DEATH FEOM 

VIOLENCE AND SUDDEN DEATH:— AND THE 

METHODS OF PEESEEVING AND EXAMINING 

PATHOLOGICAL TISSUES. 



J 



CHAPTER I. 

THE METHOD OF MAKING POST-MORTEM 
EXAMINATIONS. 

General Considerations. 

The object in making a post-mortem examination may be to deter- 
mine whether a person has died from violence or poisoning ; to account 
for a sudden death ; or to study the lesions of disease. In any case the 
examination should include all the inij)ortant loarts of the body, not 
merely a suspected organ, and the results should be recorded at the time 
the examination is made. 

Great care is necessary in endeavoring to ascertain the cause of death 
when the clinical history is imx^erfect or unknown. Mechanical injuries, 
which destroy life by abolishing the function of one of the important 
viscera, are relatively infrequent. Most of the lesions found after death 
are rather the marks of disease than the cause of death. We do not 
know, for exami)le, how great a degree of meningitis, or of pneumonia, 
or of endocarditis, or of cirrhosis, or of nephritis necessarily leads to 
death. On the contrary, one patient may recover with an extent of 
lesion which is sufficient to destroy the life of another. So with acci- 
dents ; there is often no evident reason why fractures of the skull or of 
the pelvis should destroy life, yet they usually do. In some of the in- 
fectious diseases, such as typhoid fever, the visible lesions cannot always 
be called the cause of death. Sudden deaths of persons apparently in 
good health are often ]Darticularly obscure. In many of them we have 
to acknowledge that we can find no sufficient cause for the death. This 
is of course due to our imperfect knowledge, but it is much better in 
such cases to avow ignorance than to attribute the death to some trifling 
lesion. The brain and the heart are the organs which are especially cap- 
able of giving symptoms during life, without corresponding lesions after 
death. Very well-marked cardiac or cerebral symj^toms may continue 
for days or months, and ax3parently destroy life, and yet after death 
we find no corresponding anatomical changes.' But it should be re- 
membered that recent advances in our knowledge of the cell, which an 
improved technique in hardening and preparation has greatly fostered, 
have already shown that under various abnormal conditions the cells, 
especially of the nervous system, may undergo morphological changes of 
great significance, without perceptible alteration in the gross appearance 

1 See Sudden Death, page 49. 



4 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

of the affected part, changes which even the microscopical examinaijons 
of the past have failed to disclose. So that while there often appear^ to 
be a wide discrepancy between symptoms and lesions, with the increase 
of knowledge the scope of this discrepancy is steadily narrowing. It is 
the novice in post-mortem examinations who is particularly apt to mis- 
take ordinary post-mortem alterations for significant lesions. 

External Inspection. 

Before commencing the examination of the internal viscera an in- 
spection should be made of the external surface of the body. The mi- 
nuteness of this inspection will depend upon the character of the case. 
In the case of an unknown person, or of one suspected to have died 
from unnatural causes, it is necessary to search for and record not only 
all contusions, wounds, etc., their size, situation, and condition, but also 
deformities from disease and any physical peculiarities of hair, eyes, 
teeth, moles, etc. , by which the person may be identified. In such cases 
it is well, if possible, to photograph, weigh, and measure the body. In 
cases of doubtful identity it is sometimes wise to make a wax or plaster 
cast of the outside of the teeth and jaws. In ordinary examinations we 
note the general nutritive condition of the body, and look for evidences 
of external injury, for skin diseases, ulcers, oedema, gouty deposits, ab- 
scesses, enlarged lymph nodes, etc. The external organs of generation 
should be searched for syphilitic lesions. 

It is usual to find certain changes in the external appearances of the 
body, which are due to the cessation of life and the commencement of de- 
composition. We speak now of bodies which have not been buried, but 
which have been kept in the ordinary way, lying on the back, and loose- 
ly covered with a shroud or dressed with the ordinary clothing. 

Weight. — It is well to weigh the body in all cases. There is of course 
large variation in the weight of individuals within the limits of the nor- 
mal. But the averages may be useful in estimating the relative weight 
of single organs. 

Cadaveric Lividity. — After life becomes extinct, and before the blood 
coagulates, it changes its position chiefly in two ways : first, it is driven 
by their contraction out of the arteries into the veins ; second, it settles 
in the veins and capillaries of the more depeiident parts of the body, in- 
ducing, usually within a few hours after death, a mottling of the surface 
with irregular livid patches. These patches may coalesce, forming a 
uniform dusky-red color over the back of the trunk, head, and extremi- 
ties, and sometimes over the ears, face, and neck. The same effect is 
observed on the anterior aspect of the body if it has lain on the face. 
At points of pressure, from folds in the clothing, or from the weight of the 
body on the table, the red color is absent or less marked. These changes 
occur before putrefaction sets in. This cadaveric lividity or hypostasis 
should not be mistaken for ante-mortem ecchymosis, from which it may 
usually be readily distinguished by its position and extent, by the fact 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 5 

that tlie surface of the skin is not elevated, and by the fact that on in- 
cision no blood is found free in the interstices of the tissues. Not infre- 
quently the subcutaneous tissue in the vicinity of these post-mortem 
hypostases becomes infiltrated with reddish serum. Yery soon after 
death, particularly in warm weather, the tissues immediately around the 
subcutaneous veins of the neck and thorax, and in other situations, may 
become stained of a bluish-red color from the decomposition and escape 
from the vessel of the coloring matter of the blood. If the epidermis 
has been detached at any point, the skin beneath soon becomes dry and 
brown. 

Putrefactive Changes. — Usually in from one to three days, depending 
ui^on circumstances, a greenish discoloration of the skin appears, at first 
upon the middle of the abdomen, over which it gradually spreads, as- 
suming a deeper hue and often changing to a greenish purple or brown. 
Greenish patches may now appear on different parts of the body, earliest 
u]Don those overlying the internal cavities ; this discoloration is probably 
produced by the action on the hsemogiobin of gases developed hj decom- 
position. The eyeballs now become flaccid, and if the eyelids are not 
closed the conjunctiva and cornea become brown and dry. The pressure 
of gases developed by decomposition in the internal cavities not infre- 
quently forces a greater or less quantity of frothj^, reddish fluid or mu- 
cus from the mouth and nostrils, distends the abdomen, and, if excessive, 
may lead to changes of position of the blood in the vessels, and even a 
moderate amount of disi)lacement of the internal organs. 

After five or six days, under ordinary circumstances, the entire sur- 
face is discolored to a green or brown. After this the epidermis becomes 
loosened through the formation of gases and separation of fluids beneath, 
and the tissues become flaccid. The abdomen and thorax may be greatly 
distended, the features distorted and scarcely recognizable from swelling, 
and the hair and nails loosened. Beyond this stage of putrefaction the 
consecutive changes, leading to more or less disintegration of the soft 
tissues, can scarcely be followed with certainty. The rapidity with 
which these changes follow one another depends upon a variety of con- 
ditions, such as temperature, moisture, access of air, and the diseases 
which have preceded or caused death. Thus an elevated temperature 
and the x>resence of air and moisture hasten the advent and progress of 
putrefactive changes. The bodies of infants usually decompose more 
rapidly than those of adults, fat bodies more quickly than lean ones. 
The infectious diseases, intemperance, and the puerperal condition pro- 
mote rai^id decomposition, as does also death from suffocating gases. 
Poisoning by arsenic, alcohol, antimony, sulphuric acid, strychnin, and 
chloroform may retard the progress of decomposition. Burial in dry 
soil and submersion in water also retard the progress of decay. ' 

Cooling of the Body. — The internal temperature of the healthy living 

^ References to the relationship of bacteria to the putrefaction of dead bodies and a 
discussion of certain medico-legal phases of putrefaction may be found in Babes, "Les 
maladies infectieuses en medecine legale," Annales d'Hygi^ne Publique, March, 1899. 



6 THE METHOD OF MAKIIS^G POST-MOETEM EXAMINATIONS. 

body is about 37.2° C. (99° Fahr. ). But it maybe increased several 
degrees in consequence of disease. After death the chemical changes 
upon which the maintenance of this temperature depends rapidly dimin- 
ish, and the body gradually cools to the temperature of the surrounding 
medium. This usually occurs in from about fifteen to twenty hours, but 
the time required depends upon a variety of conditions. Immediately 
after death there is, in nearly all cases, a slight elevation of internal 
temperature, owing to the fact that the metabolic changes in the tissues 
still continue for a time, while the blood ceases to be cooled by passing 
through the lungs and perii^heral capillaries. After death from certain 
diseases — yellow fever, cholera, rheumatic fever, and tetanus — a consid- 
erable elevation of internal temperature has been repeatedly observed. 
The time occui)ied by the cooling of the body may be prolonged after 
sudden death from accidents, acute diseases, apoplexy, and asphyxia. 
A number of cases is recorded in which the body retained its heat for 
several days, without known cause. 

After death from wasting chronic disease, and in some cases after 
severe haemorrhages, the cooling of the body is very rapid, the internal 
temperature being reduced to that of the surrounding air within four or 
five hours. Fat bodies cool less quickly than lean ones, the bodies of 
well-nourished adults less quickly than those of children or old persons. 
The temperature of the surrounding medium, the degree of protection of 
the body from currents of air, of course, modify the progress of 
cooling ; and the internal organs naturally retain their heat longer than 
the surface of the body. The rate at which cooling occurs is most rapid, 
as a rule, during the hours immediately following death, notwithstand- 
ing the post-mortem rise which may ensue. 

It will thus be seen that, if required to pronounce upon the time 
which has elapsed since death in a given case, we can do so only approxi- 
mately. It is necessary to take into account all of the above-mentioned 
conditions which modify the rate of cooling of the body, and then we 
may be able to state only the probabilities of the case. It is furthermore 
unsafe in any case to infer the cause of death from the rate of cooling of 
the body. 

Rigor Mortis. — Death is usually succeeded immediately by a period of 
complete muscular relaxation. The jaw drops and the limbs become 
flaccid. The muscles may retain for two or three hours, however, the 
capacity of contracting, on the application of appropriate stimuli. On 
the average, within six hours the muscles become firm and rigid. This 
post-mortem rigidity is called rigor mortis. On the occurrence of the 
rigor mortis the muscles become fixed in whatever position they may 
have had at the time of its occurrence. It usually begins in the muscles 
of the eyelids, extends to those of the back of the neck and lower jaw, 
then to the face and neck, and thence passing downward affects the mus- 
cles of the thorax and lower extremities. It usually disappears in the 
same order. Although commencing on the average six hours after death, 
it may set in at once or be delayed for twenty -four hours or more. It 



THE 3IETH0D OF MAKIXG P0ST-3I0ETEM EXAIMIXATIOXS. 7 

may pass off very rapidly, in rare cases in from oue to three hours ; or 
it may persist for two or three weeks or longer. It may be said in gen- 
eral that the average time of its disappearance is within twenty-fonr or 
forty-eight honrs after its occurrence, depending on temperature, its 
intensity, the mode of death, the period of its advent, etc. Caspar 
states that in foetuses before term he has never observed rigidity, and 
that in young children it is feeble and of short duration. Its occurrence 
and phenomena may be in some cases of the highest medico-legal imjior- 
tance ; but its careful observation does not, with our x^resent knowledge 
of its significance, appear essentially to further the aims of the practical 
pathologist. ' 

Contusions. — It is often important to determine whether violence has 
been inflicted upon a body before death. In regard to this point, we 
must remember, first, that blows and falls of sufficient violence to frac- 
ture bones and rupture the viscera may leave no marks on the skin, even 
though the person has survived for several daj'S ; and, second, that there 
are post-mortem ax)pearances which simulate ante-mortem bruises. A 
severe contusion during life may present, at first, no mark or only a 
general redness. After a short time the injured part becomes swollen 
and of a red color ; this color may be succeeded by a dark blue, and this 
in turn fade into a greenish yellow or yellow ; these later appearances 
are due to an escape of blood from the vessels and to a subsequent de- 
comx^osition of haemoglobin. If therefore we cut into such an ecchy- 
mosis after death, we find extravasated blood or the coloring matter of 
the blood, in the form of pigment granules, free in the tissues. Post- 
mortem discolorations, on the other hand, although their external ap- 
X^earance may resemble that of ante-mortem ecchymosis, are not formed 
by ah extravasation of blood, but by a circumscribed congestion of the 
vessels or by an escax)e of blood-stained serum. If we cut into such dis- 
colorations, therefore, we find no blood outside the vessels. Care should 
be taken not to mistake the lesions of hsemorrhagic infection for trau- 
matic ecchymoses. 

Blows on the skin of a bodj' which has been dead for not more than 
about two houi^s may x^i'oduce true ecchpnoses with extravasation of 
blood, such as can be distinguished with great difficulty or not at all 
from those formed during life. If x^utrefactive changes be present, the 
difficulty of distinguishing between ante-mortem and x^ost-mortem bruises 
is greatly enhanced. 

Hanging and strangulation are attended with the formation of marks 
on the neck which are described in works on forensic medicine. These 
marks must not be confounded with the natural creases of the skin of 
the neck. 3Iany adults during life have creases of the skin of the neck, 
one or more in number, running downward from the ear under the chin 
or encircling the neck. After death these creases may be much more 

' For further details concerning rigor mortis, putrefactive changes, particularly the 
later stages, and the phenomena of cooling of the body, see Tidy, "Legal 3Iedicine," 
vol. i., or other works on medical jm-isprudence. 



8 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

evident than during life, and may be rendered more decided by the posi- 
tion of the head and the freezing of the body. They usually persist 
until the skin putrefies. 

Wounds. — We should notice the situation, extent, and direction of a 
wound, the condition of its edges and the surrounding tissues. If it be 
a deep, penetrating wound, its course and extent should be ascertained by 
careful dissection rather than by the use of a probe. 

If the edges of a wound be inflamed and suppurating, or commencing 
to cicatrize, it must have been inflicted some time before death. In a 
wound inflicted a short time before death, the edges are usually everted ; 
there may be more or less extravasation of blood into the surrounding 
tissues, and the vessels contain coagula; but sometimes none of these 
changes are observed. The chief characteristics of a wound inflicted 
after death are absence of a considerable amount of bleeding, non-re- 
traction of the edges, and the absence of extravasation of blood into the 
tissues. But a wound inflicted within two hours after death may resem- 
ble very closely one received during life. In general, unless a wound is 
old enough for its edges to present inflammatory changes, we must be 
very careful in asserting its ante-mortem or post-mortem character. 

Fractures. — It may be im]3ortant to determine whether a bone was 
fractured before or after death. This point cannot always be decided. 
Fractures inflicted during life are, as a rule, attended with more extrava- 
sation of blood and evidences of reaction in the surrounding tissues ; but 
fractures produced within a few hours after death may resemble these 
very closely. Usually a greater degree of force is necessary to fracture 
bones in the dead than in the living body. 

Scars and Tattoo Marks. — The presence and character of cicatrices 
should be noticed. Scars produced by any considerable loss of substance 
may become very much smaller and less conspicuous, but never entirely 
disappear. Slight and superficial wounds, however, leave marks which 
may not be permanent. The discoloration produced by tattooing may, 
although it rarely does, disappear during life. 

Internal Examination.' 

After completing the external inspection of the body, we commence 
the internal examination. In order that this examination may be made 
both thoroughly and rapidly, we should follow a regular method. The 
method should be such as will enable us to examine the relations of parts 
to one another, without seriously disturbing them, and to remove and 
inspect the organs in such an order and manner as will not interfere with 
the examination of parts which are to follow. In certain cases it may 
be necessary to depart from the regular method; but, as a rule, the 
following plan will be found most advantageous. 

^ Absolute and relative sizes and weights of various parts and organs of the body, 
and mucli other valuable statistical data, may be found in Vierorclfs " Anaiomische, 
Physiologische und Physikalische Daten und Tabellen," Jena, 1893. 



THE METHOD OF MAKIXG POST-:\IOETEM EXAMIXATIOXS. 9 

It is important to remember the difference between the distribution 
of the blood in the bodj' during life and after death. During life the 
blood is in constant motion and is distributed in a regular way in the 
heart, capillaries, arteries, and veins. Inflammations and obstructions 
to the circulation may disturb this natural distribution and produce con- 
gestion of particular parts of the body. After death the blood ceases to 
circulate ; it leaves the left cavities of the heart, the arteries and capil- 
laries, and collects in the veins and the right cavities of the heart. Ac- 
cording to the character of the disease which causes death, coagulation 
of the blood takes place more or less extensively and at an earlier or 
later x)eriod. The local congestions which existed during life often dis- 
appear after death. On the other hand, local congestions are found after 
death which did not exist during life. Thus, after death the scalp often 
contains a large amount of venous blood. The veins of the pia mater 
and the sinuses of the dura mater may be filled with blood. The mucous 
membrane of the larynx and trachea may appear to be deeply congested. 
The lungs are congested if the patient has been comatose for some hours 
before death. All the tissues of the back and the membranes of the 
spinal cord are often gorged with venous blood. The right auricle and 
ventricle of the heart may contain fluid or clotted blood in considerable 
quantity. 

THE HEAD. 

The scalp is divided by an incision across the vertex, from ear to ear. 
The flaps are dissected forward and backward, taking up the temporal 
muscles with the skin and leaving the x)ericranium attached to the bone. 
The internal surface of the scalp and the x)ericranium are to be searched 
for ecchymoses and inflammatory lesions. 

A circular incision is now made through the cranium with a saw. 
The incision should, in front, pass through a point about three and one- 
half inches above the bridge of the nose ; behind, through the occipital 
protuberance. Care should be taken not to cut through the dura mater 
with the saw. ^Tien the roof of the cranium is thus entirely loosened, 
a stout hook is introduced under the uiDper edge of the calvarium, and 
this is wrenched off with a jerk. 

Sometimes the dura mater is so firmly adherent to the calvarium that 
the latter cannot be torn from it without injury to the brain. In this 
case, and also if the dura mater should have been accidentally cut 
through by the saw in making the circular incision, the dura mater may 
be cut through at the level of the cranial incision, and the brain removed 
with the calvarium and separated afterward. Or, which is better, in 
addition to the circular incision, a longitudinal incision is made, from 
front to back, about three -cpiarters of an inch to one side of the median 
line of the skull, and a segment of bone removed. The knife blade may 
now be inserted from the open side, and the dura cut away from the 
skull-cap along the line of the longitudinal sinus, where the adhesions are 
apt to be most firm. 



10 THE METHOD OF MAKING POST-MOETEM EXAMINATIONS. 

We should notice whether or not the calvarium is symmetrical. The 
cranial bones increase in size by a growth of bone at the edges of the su- 
tures. If any suture become completely ossified and closed prematurely, 
the bones will be unequally developed. The thickness and density of 
the cranial bones vary considerably within the limits of health. There 
are often deep depressions on the inner surface of the skull along the 
sagittal suture, caused by the pressure of the Pacchionian bodies, and of 
no pathological significance. We should observe the blood content of 
the bone, determine the existence or absence of fractures, inflammatory 
lesions, exostoses, etc. 

The Dura Mater is now exposed. It is more or less adherent to the 
calvarium ; a moderate amount of adherence, especially in old persons, 
does not denote disease. Very extensive and firm adhesions are usually 
produced by inflammation. Near the median line the Pacchionian bodies 
often project through the dura mater and may produce indentations in 
the internal surface of the calvarium. We must look for clots and for 
tumors and for inflammatory lesions on the external surface of the dura 
mater. The longitudinal sinus should be laid open and its contents ex- 
amined. A circular incision is then made through the dura mater in a 
line corresponding to the cranial incision ; the falx is divided between 
the anterior lobes of the brain, and the entire membrane drawn back. 
We should observe the existence of abnormal adhesions of the dura mater 
to the pia mater, bearing in mind that a moderate amount of adhesion 
along the longitudinal fissure is normal. The internal surface of the 
dura mater is to be examined for the ]Droducts of inflammation and for 
tumors. 

The Pia Mater covering the convex surface of the brain is now ex- 
posed. The degree of congestion, and the existence of serum, pus, or 
blood, beneath, within, or ujDon it, are now to be ascertained before the 
brain is removed. The pia mater in old persons frequently loses its 
transparency and becomes thick and white ; this change is most marked 
along the longitudinal fissure and large vessels. Marked and general 
thickening of the pia mater is the result of chronic inflammation. Along 
the longitudinal fissure, and sometimes at a considerable distance from it, 
we usually find small, elevated, whitish nodules, which are the Pacchio- 
nian bodies and are normal in the adult. 

The amount of serum beneath the pia mater varies. A considerable 
amount, especially in cachectic persons, may exist without brain disease. 
Clear serum, raising the pia mater and separating the convolutions of the 
brain, may be simply droi)sical or due to chronic meningitis. Turbid 
and purulent serum, beneath and in the pia mater, is due to acute 
or chronic meningitis. The degree of flatness of the surface of the 
convolutions should be observed before removing the brain ; for, when 
marked, it affords an important indication of pressure, from haemorr- 
hage, inflammatory products, internal fluid effusions, and tumors. The 
pia mater should be carefully examined for miliary tubercles. 

The Brain. — After examining the convex surface of the brain, the an- 



THE METHOD OF MAKING POST -MORTEM EXAMIXATIOXS. 



11 



terior lobes of the cerebrum are to be pulled gently backward, the 
nerves, vessels, and tentorium severed, and the medulla cut squarely 
across, as low down as i30ssible. The brain is now removed from the 
cranium by passing the fingers of one hand down, beneath, and behind 
the lobes of the cerebellum, and drawing the brain out, supi^orting the 
convexity with the other hand. 

The adult brain in the male weighs on the average about 1,400 grams; 
that of the female, about 155 grams less. The average proportional 




Fig. 1.— Side View of the Human Brain, Showing its Fissures and Convolutions 



weight of the brain to that of the body is about one-forty-fifth, although 
in this, as in the absolute weight, there is considerable variation. 

The exact situation of any lesion which is apparent externally should 
be described by its relation to the lobes, fissures, convolutions, and sulci 
(Fig. 1). 

The brain is first laid uj)on its convex surface, and the anterior, mid- 
dle, and x^osterior cerebral arteries, as well as the basilar and the 
carotids, are to be examined for emboli, thrombi, atheroma, and aneur- 
isms. Evidence of extravasations of blood, tumors, and inflammatory 
lesions are now to be looked for. The brain is next turned over on to 
its base. An incision is made through the pia mater, over the convex 
surface of the cerebrum. The membrane is stripped up, and its adher- 
ence to the brain and its thickness are noted. 

The more common method of opening the brain is as follows : The 
halves of the cerebrum are to be separated until the su]3erior surface of 
the corj)us callosum is exposed (Fig. 2). A longitudinal incision is 
made through the junction of the corpus callosum and the cerebrum, and 
downward into the ventricle. The incision should be made carefully, so 
as not to cut through the ventricle into the ganglia below. The incision 



12 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 



thus made through the roof of the ventricle is prolonged backward and 
forward in the direction of the cornua, so as to expose the entire ventri- 
cle. A longitudinal incision is then made outward and backward into 
the hemisphere, from the outer edge of the lateral ventricle nearly to 
the pia mater. A second incision is then made through this cut surface 
outward, and this is repeated until the hemisphere is divided into a 




Fig. 2.— Method of Opening the Brain, Showing the Direction of First Incision. 



number of long, prism-shaped pieces, held together by the pia mater 
and a small portion of the cortex. The brain is now turned around so 
as to bring the other hemisphere under the hand, and the operation is 
repeated on the other side. 

The size, shape, and contents of the ventricles should be noticed, and 
the thickness and appearance of the ependyma. 

The fornix and the central portion of the corpus callosum are cut 
across by passing the point of the knife through the foramen of Munro 
and cutting upward. They are then drawn backward, one of the pos- 
terior cornua of the fornix being severed and laid to one side. The 



THE METHOD OF MAKIXG POST -MORTEM EXAMIXATIOJ^S. 



13 



velum interposituin and the choroid plexus are now dissected uj), the 
blood contents and the general appearance noted, and the third ventricle 
examined, ^ot infrequently small cysts of the choroid are found, which 
seem to have little or no pathological significance. 

The fourth ventricle is now opened by a longitudinal incision through 
the vermiform process. Each hemisphere of the cerebellum is divided 
first into two parts, by an incision through the upper and inner convex 
border, and then each segment is further divided by incisions in the 
same direction. 

Thin transverse sections are now made through the cerebral ganglia, 
commencing in front (Fig. 3). The ganglia are supported, and the sec- 




FlG. 3.— METHOD OF OPENING THE BRAIN, SHOWING THE UNFOLDED SEGMENTS OF THE CEREBRUM 

AND Lines of Transverse Incision of the Basal Ganglia and Directions of the Incisions of 
THE Cerebellum. 



tions caused to fall apart as they are cut, by carrying the fingers of one 
hand under the brain, and gently lifting the ganglia at points just be- 
neath where the sections are made. It is important to observe the exact 
position of any lesion which may be discovered in the cerebral ganglia, 
their relations to the external and internal capsule and to the caudate 
and lenticular nuclei. 

Finally, the segments of the cerebrum and cerebellum are folded up 
together into their original positions, the whole is turned over on to the 
vertex, and thin sections are made through the medulla. Small clots in 
the medulla should not be overlooked. 

In case of the discovery of apoplectic clots, areas of softening, etc. , 
either in the hemispheres or in the basal ganglia, after their location and 
extent are determined, they should be carefully searched for lesions of 



14 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 



the blood-vessels, minute aneurisms, areas of degeneration, and rup- 
tures. For this purpose it may be necessary to allow a stream of water 
to run over the affected portion, so as to wash out the brain substance 
and expose the vessels. In some cases the blood-vessels are best exposed 
by macerating the brain tissue at the seat of the lesion for some hours in 
water, and then washing out the brain substance under the faucet. 

While the above mode of dissecting the brain gives a very complete 
view of the seat and extent of lesions in general, when a more exact 
localization of lesions with a microscopic examination is to be made, the 
following — called Meynert's method — is a better method of opening the 
brain : 

After completing the external examination, as detailed above, the 
brain is laid on its vertex, the cerebellar end toward the operator. The 

cerebellum is raised by the 
fingers of the left hand, and 
the pia cut through along 
the sides of the corpora 
quadrigemina, around the 
crura and along the inner 
margins of the temporal 
lobes, to the middle cerebral 
artery on both sides (Fig. 4). 
Then, raising the temporal 
lobes, in turn, by their 
apices, the pia is cut through 
along the course of the mid- 
dle cerebral artery into the 
Sylvian fissure, and along 
the course of its posterior 
branch to its end. ISTow, 
drawing the temporal lobes 
one after the other upward 
and outward, their junction 
with the base is cut, the 
knife being held horizontally so as not to injure the basal ganglia, until 
the descending horn is opened. The point of the knife being in the 
descending horn, the incision through the brain substance then passes 
outward and backward well into the posterior horn, thus partially sever- 
ing, at the lateral surface of the brain, the junction of the occipital and 
temporal lobes. The temporal lobes are then turned outward and back- 
ward (Fig. 4). 

The operculum is now pulled well outward, completely exposing the 
island of Eeil, and a slightly curved transverse incision is made, deep 
enough to pass into the anterior horns of the ventricles, connecting the 
anterior sulci of the island of Eeil (Fig. 4, A, B). 

E'ow raising the cerebellum and inserting the point of the knife into 
the ventricle, with short incisions from within outward, cut through the 




Fig. 4.— Schematic Picture of Brain, Showing the Meth- 
od OF Dissection from the Base (Meynert's method). 
E and F, Temporal lobes turned backward and outward ; A 
B, A C, B D, line of Incision to remove basal piece. 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 



15 



internal capsule on either side from back to front (Fig. 4, C A and D B) 
care being taken not to injure the basal ganglia. Then cut across the 
crura of the fornix and the septum lucidum, 
leaving the fornix lying on the corpus cal- 
losum. 

The square basal piece (Fig. 5) thus freed 
— the brain axis — includes the island of Eeil, 
the basal ganglia, the crura, pons, medulla, 
and cerebellum. The remaining portion^ 
the brain mantle — includes the convolutions, 
corpus callosum, and fornix (Fig. 6). 

The basal piece may be further examined 
by a series of transverse incisions, from one- 
half to three-quarters of an inch apart, and it ^ ^ 

^ . . ^ Fig. 5.— The Brain axis Sepa- 

may be hardened either with or without the rated from the brain mantle, 
cerebellum. The convolutions may be cut ^^ ^^^^ ^^^^^ above. 
into small pieces by longitudinal and transverse incisions, made from 
within and not' reaching quite to the pia mater, which will then serve 
to hold the pieces together in their proper relations to one another. ' 





-The Brain Mantle, as Seen from Below. 
A, Internal capsule ; B, operculum ; C, posterior border of corpus callosum ; D, descending horn ; 

E, cornu ammonis. 

The Base of the Cranium. — We now return to the skull. The re- 
maining sinuses of the dura mater should be opened, and this membrane 
then entirely stripped from the bone. The bones at the base of the skull 

' For further details of this method of opening the brain and a consideration of its 
advantages, see Van Gieson, "Laboratory Notes," etc., New York Medical Journal, 
July 20th, 1889. 



^ 



16 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

are to be examined for fractures, inflammatory lesions, and tumors. In 
cases of acute purulent meningitis, the temi^oral and frontal bones should 
be carefully examined, as the inflammatory process is sometimes trans- 
mitted from the internal ear, or mastoid cells, or frontal sinuses. 

The eyes may be removed by breaking the roof of the orbit with a 
hammer, removing the fragments of bone, and dissecting away bone and 
muscles, so as to expose the optic nerve and posterior segment of the 
eye. That portion of the globe which is not covered by conjunctiva can 
now be cut away with scissors and removed with the optic nerve, or, 
when permissible, the whole eye may be cut out. 

The examination of the internal ear may be made by removing its 
entire bony encasement with the saw and chisel, or by the exposure of 
special parts by hammer and chisel, and by suitable opening of the re- 
moved parts with a fine saw. 

Hardening and Preservation of the Tissues for Microscopical Examination. 

For the study of tumors and inflammatory lesions of the bones of the skull and 
ossifications of the dura mater and pia mater, the affected portions should be cut into 
small pieces, fixed in five-per-cent. formalin or in Orth's fluid, see page 53, and decalci- 
fied. The dura mater should be stretched on a flat piece of wood or cork with pins, 
before hardening.^ 

The _pm mater is so delicate that if it be separated from the brain when quite fresh 
its tissues are apt to be injured. The portions of the pia mater which are to be pre- 
served should therefore be removed by cutting off slices of the brain substance about 
half an inch thick, with the membrane still attached, and placing the whole in Orth's 
fluid. After twenty-four hours, the pia mater will have become sufficiently hard to 
permit of its being stripped off without injury, and it is then spread loosely on a flat 
cork with pins, the free surface outward, and the cork floated, specimen side down, in 
eighty-per-cent alcohol, changing to strong alcohol after twenty-four hours. 

Wh(*n sections are required showing the pia in its relationship to the underlying 
brain tissue, small blocks of the brain and pia together should be cut out and hardened 
in Orth's fluid or in formalin (5 : 100) solution (see page 53). 

When the ependyma is to be studied apart from the associated nerve tissue, it may 
be sliced off with a sufficient quantity of underlying brain substance to prevent its fold- 
ing, and hardened in Orth's fluid. The hrain, for general purposes, may be hardened 
in Orth's fluid or in five-per-cent formalin. The pieces of brain tissue should not be 
more than 1 cm. thick; it is better if they are thinner than this. They should be sus- 
pended in gauze or rest upon a layer of absorbent cotton on the bottom of the jar, the 
pieces, if these are numerous, being held apart by a little cotton. Thus the preserva- 
tive fluid which should be abundant, is in contact with the surfaces of the pieces of 
tissue. Ordinarily, with a change of fluid on the second day, the fixation by formalin 
or Orth's fluid is complete in a week, when the fixatives are thoroughly washed out and 
replaced by fifty-per-cent alcohol, which, in turn, is replaced after forty-eight hours by 
eighty-per-cent or by ninty-five-per-cent alcohol. 

When degeneraiion in nerves is to be studied, the specimens of nerve tissue may, 
by Marchi's method, be hardened for a week in Mliller's fluid, and then transferred to 
the following solution: 

Mliller's fluid, 2 parts. 

Osmic acid, one per cent 1 part. 

After a week the specimens are washed and transferred to ninety-five-per-cent 
^ For details of the methods of hardening, decalcifying, staining, etc. , see page 52. 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 17 

alcohol. In such specimens the fat droplets in the degenerate areas are black, while 
the myelin is yellowish in color. 

Certain lesions, particularly the softenings of the brain, are best studied by teasing, 
when fresh, in one-half-per-cent solution of sodium chloride, or in frozen sections of the 
fresh tissue. The blood-vessels may be stretched on cork with pins and hardened with 
Ortli's fluid or formalin. The eye and portion of the optic nerve, if removed, should 
be fixed by Orth's fluid and the hardening completed by alcohol. 

For many methods of fixation and study which are useful for special purposes, we 
refer to special works on technique. 

THE SPINAL CORD. 

The examination of the spinal cord is usually most conveniently made 
after the removal of the brain. 

The body should be placed face downward, with a block under the 
thorax and the head hanging over the edge of the table. An incision is 
made through the skin and muscles along the entire length of the spine, 
and the soft parts are dissected away on each side so as to expose the 
laminse of the vertebral column. The laminge are then divided, close 
within the articular processes, with the saw. 

The saw should be so directed in severing the laminae that the inci- 
sion shall touch the outer border of the spinal canal, as otherwise the 
laminae and spinous processes are not easily separated. Great care 
should be taken on the one hand not to injure the cord with the saw, 
and on the other completely to loosen the j^ortious of bone to be removed. 
These, which are the spinous processes and laminae, are now torn away 
together, with a stout hook, exposing the cord. 

By means of a long, curved chisel, made for this purpose, the bodies 
of the vertebrae may be removed from the front after the thoracic and 
abdominal viscera are taken out, and the cord thus exposed and re- 
moved. But in this anterior method of removing the cord, as well as by 
the use of chisel and mallet, bone shears, etc. , in the ordinary method, 
there is great liability of injuring the delicate tissues of the cord and 
producing, as Yan Gieson has shown,' mechanical - alterations which are 
likely to be mistaken for malformations or the results of disease. 

When the body has lain on the back, the membranes of the cord may 
be found considerably congested, without indicating the pre-existence of 
disease. If the body has lain for some time, epecially in warm weather, 
serous fluid may have accumulated within the membranes, as a result of 
post-mortem change. 

The roots of the nerves are now to be cut across, as far away as pos- 
sible from the cord, and the cord removed in its membranes, care being 
taken not to press it in any way. It is the safest plan not to grasp the 
cord itself, but with a forceps to seize the dura mater and thus lift it up 
at once as it is freed from its attachments. It is now laid on the table, 
and the dura mater laid open with scissors on the anterior and posterior 
surfaces over its entire length, and searched for tumors, inflammatory 

^ Van Gieson, "A Studv of the Artefacts of the Nervous System," New York Med- 
ical Journal, vol. Ivi., pp. 337, 365, 421. 1892. 
2 



18 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 



lesions, etc. The finger should be passed gently along the cord as it lies 
on the table, so as to detect any marked softening or sclerosis. The 
weight of the spinal cord is from 30 to 38 grams. It should now be held 
lightly over the fingers, and smooth transverse incisions made, with a 







Fig. 7.— Outlines of Sections of the Spinal Cord at Different Levels. 
Copies of these outlines may be used for memoranda of the situation of lesions of the spinal cord. J, 
Second cervical ; II, fifth cervical ; III, eighth cervical ; IV, first dorsal ; V, eighth dorsal ; VI, third 
lumbar ; VII, fourth sacral. 



very sharp knife or razor, about half an inch apart through its entire 
substance between the segments, leaving these attached to the pia mater. 

The segments of the spinal cord are those parts from which the spi- 
nal nerves arise, and it is convenient for the location and description of 
lesions to number the segments in correspondence with the nerves which 
arise from them and to indicate on outline diagrams of the cord (Fig. 7) 
the exact seat of small lesions. 

The cut surfaces should be carefully examined for abnormal blood 
contents, haemorrhages, inflammatory lesions, softening, scleroses, and 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 19 

pigmentations. Important lesions of tlie cord may be invisible to the 
naked eye, and hence, if disease be suspected, the organ should be pre- 
served for microscopical examination. The spinal ganglia may now be 
removed and i)reserved for further examination. After removal of the 
cord, fractures and displacements of the vertebrae are easily recognized. 

Preservation of the Spinal Cord and its Membranes, and of Peripheral 
Nerves. — After the removal of the spinal dura, the entire cord with its nerve roots — 
the segments into which it has been cut for gross examination being left in place — should 
be laid on a wad of absorbent cotton in a large jar of Orth's fluid or formalin, the seg- 
ments being slightly separated from each other by a little absorbent cotton. Van Gie- 
son recommends the careful rolling of the segmented cord into a loose spiral and laying 
this coil on a wad of absorbent cotton in the fixative. In this way the cut ends of the 
segments are held apart, accessible to the fluid, and harden with little distortion. 

The hardening and preservation of the cord may be done by the same methods as 
suggested above for the brain. If the dura mater of the cord alone is to be preserved, 
it should be treated in the manner suggested for the dura mater cerebralis. The pia 
mater spinalis is best studied in sections through the entire cord, the membranes being 
left in situ. 

Peripheral nerves may be hardened in Orth's fluid or in formalin. 

For the hardening of the peripheral nerves, osmic acid is very useful, especially 
when changes in the myelin are to be sought after. As osmic acid does not readily 
penetrate the lamellar sheath so as to come in contact with the nerve fibres, in trunks 
of any considerable size, the following procedure, as suggested by Van Gieson, will be 
found useful: A piece about one-half inch long is cut from the nerve to be examined: 
one end of this segment is held with a forceps, while with another forceps the individual 
nerve fibres, or small clusters of these, are pulled, out of the lamellar sheath and put at 
•once in a one-per-cent aqueous solution of osmic acid, in which they remain twenty-four 
hours, and are then washed and transferred to glycerin, to which twenty-five per cent 
alcohol is added. In this mixture they may be preserved. Marchi's method (see above, 
p. 16) is useful for the study of degeneration in peripheral nerves. 



THE THORAX AND ABDOMEN. 

The body is replaced on its back, and a single straight incision is 
made from the top of the sternum to the pubes, passing to the left of the 
umbilicus. For this purpose a large knife should be used, held firmly 
in the whole hand, and the movement should be mainly from the shoul- 
der. The first incision should divide everything down to the sternum 
and peritoneum. A short incision should then be made through the 
peritoneum, just below the ensiform cartilage. Into this opening two 
fingers of the left hand are introduced and separated from one another, 
and, the parietes being raised and the sides of the opening being held 
apart by the fingers, the peritoneum is divided to the pubes, care being 
taken to hold the knife horizontally so as not to cut the intestines. The 
skin and muscles are then dissected off from the thorax on both sides as 
far back as the false ribs. 

This dissection should be made by long sweeps of the knife, which 
should be made to cut with the full blade and not with the point only : 
and if the skin and muscles be pulled strongly away from the chest with 
the left hand, it may be done very rapidly and with a few strokes of the 
knife. We notice here the amount of subcutaneous fat and the condi- 



20 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

tiou of the muscles. In order better to expose the abdominal cavity, the 
rectus should be divided transversely beneath the skin just above the 
pubes, and the abdominal flaps may then be turned freely outward. 

General Inspection of the Abdominal Cavity. — We first notice the posi- 
tion and general condition of the viscera. It is best at this stage of the 
examination to note the condition of the vermiform appendix, and to 
look over the peritoneal cavity for serum, inflammatory lesions, evi- 
dences of perforation, and for the existence of invagination, incarcera- 
tion, and hernise of the intestines. A small quantity of reddish serum 
is frequently found in the abdominal cavity, particularly in warm 
weather, as the result of commencing decomposition. 

It should be remarked here that various striking changes in the 
character and appearance of the internal organs are produced by putre- 
faction — changes which are often mistakenly regarded as evidences of 
disease, and much experience is required in judging correctly of their 
significance. These changes are, in general, softening and discoloration, 
both of which may occur as the result of disease. It may be said in 
general that the post-mortem reddening, or hypostases, are most marked 
in the more dependent parts of the organs. Post-mortem softening usu- 
ally affects entire organs, not being limited to a part, as is often the case 
in disease. Gray or greenish-brown post-mortem discolorations are apt 
to appear in those organs or parts of organs which lie in contact with the 
intestinal canal. Parts of internal organs such as the liver, which have 
been the seat of localized congestion during life, may after death assume 
a dark -greenish color. 

The omentum is usually spread over the surface of the small intes- 
tines, but it may be rolled up and displaced in a variety of ways, or may 
be adherent at some point to the small intestines or the abdominal wall. 

The surface of the small intestines should be smooth and shining. 
They may be greatly distended with gas, and thus so completely cover 
the other abdominal viscera that it becomes necessary to let out some of 
the gas by a small puncture. The transverse colon passes across the 
abdomen through the upper part of the umbilical region. It may be 
lower than the umbilicus, or higher up against the liver and diaphragm ; 
it may be distended with gas or contracted. 

The liver is situated in the right hypochondriac and epigastric re- 
gions, filling the concavity of the diaphragm. Its upper border reaches, 
in the linea mammillaris, to the fifth intercostal space ; in the linea axil- 
laris, to the seventh intercostal space ; close to the vertebral column, to 
the tenth intercostal space. At the median line the upper border of the 
liver corresponds to the lower border of the heart. The left lobe extends 
about three inches to the left of the median line. The lower border of 
the right lobe usually reaches to the free border of the ribs, while the 
left lobe is visible for about an inch below the ensiform cartilage. In 
women the liver is usually lower than in men. 

The position of the liver is affected by changes in the thoracic cav- 
ity, forcing it downward ; by changes in the abdominal cavity, forcing 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 21 

it upward ; by constriction of the waist in tight lacing, forcing it either 
upward or downward ; by changes in the size of the organ itself. The 
liver may not only be displaced downward, but dislocated so that its 
convex surface faces the abdominal wall and its posterior edge is turned 
upward against the diaphragm. 

The stomach is situated in the left hypochondriac and epigastric re- 
gions, extending also into the right hypochondrium ; it lies in part 
against the anterior wall of the abdomen, in part beneath the liver and 
diaphragm, and above the transverse colon. Its anterior surface, which 
is directed upward and forward, is in contact above with the diaphragm 
and the under surface of the liver, and lower down with the abdominal 
wall opposite to the epigastric region. Its posterior surface is turned 
downward and backward, and rests on the transverse mesocolon, the 
pancreas, and the great vessels. To its lesser curvature or upper border 
are attached the gastro- phrenic ligament and the gastro -hepatic omen- 
tum. To the greater curvature or lower border is attached the gastro- 
colic omentum. Its cardiac orifice communicates with the oesophagus, 
its pyloric end with the duodenum. 

When the stomach is distended the greater curvature is elevated and 
carried forward, the anterior surface is turned upward and the posterior 
surface downward. When distended with food or gas the organ is prom- 
inent ; when emj)ty it may hardly be visible below the ribs ; when the 
intestines are dilated it may be entirely covered by them. 

Before opening the thorax the hand should be passed up against the 
under surface of the diaphragm on either side, to determine its height. 
According to Quain, the vault of the diaphragm rises, in the dead body, 
on the right side to the level of the junction of the fifth rib and sternum, 
on the left side as high as the sixth rib. Both the relative and the 
absolute height of the diaphragm vary under a variety of pathological 
conditions. 

If the existence of air or gas in the pleural cavities be suspected, the 
abdominal cavity should be filled with water and the diaphragm punc- 
tured below the level of the fluid. If air be present, it will escape in 
bubbles through the water. 

The Thorax. 

We now leave the abdominal viscera and proceed to the examination 
of the thorax. With a costatome or a strong knife the costal cartilages 
are divided close to the ribs, the clavicles are disarticulated from the 
sternum, and the latter is removed, care being taken not to wound the 
large veins. We first examine the position of the heart and lungs. 

The Heart. — The upper border of the heart is on a level with the 
third costal cartilage; the lower border extends from 1.3 cm. below 
the lower end of the sternum to the fifth left intercostal space. The 
left boundary of the heart is situated to the left of the junction of the 
fifth rib with its costal cartilage, and behind or to the left of a vertical 



22 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

line drawn downward from the left nipple. The right boundary extends 
2.5 cm. to the right of the right edge of the sternum. The portion of the 
heart uncovered by the lungs is of an irregular quadrangular shajoe. Its 
lateral diameter is from 3.8 cm. to 11.1 cm. ; its upper boundary varies 
from the level of the second costal cartilage to that of the fifth, but it is 
usually behind the third or fourth cartilage or fourth space. 

The area of the heart which is found uncovered will, however, vary 
much, according to the degree to which the lungs collapse after opening 
the chest. Any disease which diminishes the size of the lungs, or pleu- 
ritic adhesions which retract or bind them down, may increase the area 
of exposed heart. On the other hand, emphysema, pneumonia, or any 
disease which increases the size of, or retains the air in, the lungs, may 
diminish the area of exposed heart. The exposed area varies also with 
the size of the heart itself. 

The Pericardium is now opened by a slightly oblique incision on its 
anterior surface. The existence of serous, fibrinous, or purulent exu- 
date, and of adhesions, is to be noticed. A small quantity of clear serum 
exists normally in the pericardial sac, and this serum may be blood- 
stained from beginning decomposition. AVliite thickenings of the peri- 
cardium on the surfaces of the heart are often seen ; they do not indicate 
important disease. 

Now that the pericardial sac is open, the position of the heart can be 
clearly seen. It lies obliquely in the chest, its long axis at an angle of 
about sixty degrees with that of the thorax. The portion of the heart 
which is first seen is the anterior surface of the right ventricle ; upward 
and to the right of this is the right auricle, which lies about two -thirds 
on the right of the sternum and about one -third behind it. Its upper 
border usually corresponds to the iDlane of the middle of the anterior 
end of the second intercostal space on the right side. Its size varies 
with the amount of blood which it contains. The left auricle lies behind 
the root of the pulmonary artery, so that only its appendix is visible. 
The middle of the auricle corresponds to the third costal cartilage. Of 
the left ventricle only a narrow rim is seen, on the left side of the right 
ventricle. The pulmonary valve is usually entirely or in part on the 
left side of the sternum, behind the second space or third costal cartilage. 

The aortic valve is usually at the level of the third cartilage or the 
third space, and behind the left two -thirds or half of the sternum. The 
mitral valve is oblique, the upper end to the left. It is on the level of 
the third to the fourth cartilage, near the middle of the sternum. The 
tricuspid is oblique, its upper end to the left ; the upper end is at the 
level of the third cartilage, the third space, or the fourth cartilage. 
The valve is opposite the middle of the sternum. 

The hand should now be passed over the arch of the aorta, to ascer- 
tain whether or not an aneurism is present. The heart is then grasped 
at the apex, raised out of the pericardium, tilted upward, and removed 
unopened by cutting through the vessels at its base. 

To determine the sufficiency of the aortic and pulmonary valves, the 



THE METHOD OF MAKING POST-MORTEM EXAMIXATIOXS. 23 

heart is held horizontally by both auricles, so as not to pull the valves 
open, and water is poured into the aortic and pulmonary arteries, and 
we observe how well the valves suj^port the column of liquid. To ascer- 
tain the sufficieucj' of the mitral and tricuspid valves, the auricles are 
first laid open so as to expose the upper surfaces of the valves. A large 
pipe is passed through the aorta or pulmonary artery beyond their 
valves, and a small stream of water allowed to flow into the ventricles. 
The auriculo-ventricular valves will be swollen upward, and we can ob- 
serve their degree of sufficiency. The tricuspid valve is normally some- 
what insufiicient. These water tests, however carefully applied, are not 
very reliable, since under the most favorable conditions the natural 
bearings of the valves are not perfectly preserved. 

To ascertain the size of the different valvular openings, we introduce 
the fingers, held flat with their sides in contact, into each of the orifices, 
and then measure the width of the fingers at the point where they fill the 
orifice. In this way we find that, under normal conditions in the adult, 
the aortic measures about 2.5 cm., the mitral valve about 4.5 cm., the 
pulmonary about 3.1 cm., the tricuspid about 5 cm. 

In order to examine the interior of the heart, we first make an incision 
through the anterior wall of the left ventricle, close by and parallel to 
the sei^tum, and reaching to the apex of the ventricle; through this 
opening the blade of the enterotome is passed up into the aorta, the 
pulmonary artery being drawn aside with the fingers, and the ventricle 
and aorta are laid open. AVith a little care the incision may be made to 
pass through one of the points of junction of the aortic valves. 

The auricles and ventricles may be emiDty, or may contain fluid blood 
or the so-called heart elots. These heart clots are of two kinds — those 
which are formed some time before death, and those which are formed 
during the last hours of life and after death. The clots which are formed 
some time before death are usually associated with organic disease of the 
heart, especialh' with dilatation of the ventricles. They are firm, dry, 
and of whitish color; they may be infiltrated with the salts of lime. 
They are free in the cavities of the heart, or entangled in the trabecule, 
or firmly adherent to the endocardium. They are usually composed of 
coagulated fibrin, blood j)latelets, leucocytes, and red blood cells, and are 
often lamellated. The clots which are formed during the last hours of 
life and after death are red, yellow, or white. They may be soft or suc- 
culent or quite firm. They inay be free in the heart cavities, or be 
adherent to the trabeculse, or extend into the large vessels. They are 
usually most constant and of largest size in the right auricle and ven- 
tricle. Such clots may be formed within two hours after death. Clots 
of this character are common. If, then, rhe blood coagulates in the heart 
within twenty-four hours before death, this coagulum may not be dis- 
tinguishable from the ordinary post-mortem clots. If it is supposed, 
therefore, that a person dies from heart clot developed a few hours before 
death, the proof of this must be derived largely from the clinical symp- 
toms, and not from the autopsy. 



24 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

The condition of the aortic valves and of the endocardinm, and the 
thickness and appearance of the walls of the left ventricle, papillary 
muscles, chordse tendinese, etc., are now noticed. The right ventricle is 
now opened by an incision through its anterior wall, close to the septum, 
and examined in the same way. We sometimes see the endocardium of 
the upper part of the left ventricle thick and white, without the exist- 
ence of valvular lesions or any clinical history of disease. The endocar- 
dium and valves are often stained red, particularly in warm weather, by 
imbibition of coloring matter of the blood, set free by decomposition. 
To complete the examination of the cavities the enterotome is passed into 
each auricle, carried down into the corresponding ventricle, and an 
incision made along the outer border of both auricle and ventricle to the 
apex of the latter. In this way the auriculo-ventricular valves are com- 
pletely exposed. The coronary arteries should be opened through all 
their main trunks, with fine probe-pointed scissors, and carefully 
examined for marks of inflammation, emboli, thrombi, etc. 

After removing the blood the heart should be finally weighed. The 
normal average weight of the heart in adults is, according to an estimate 
of H. D. Arnold,' in males about 290 grams; in females about 260 
grams. 

The weight of the heart relative to that of the body is in males about 
1 : 158 to 178 ; in females, about 1 : 149 to 176. According to Buhl, the 
average thickness of the wall of the left ventricle at about the middle of 
the cavity is from 1.6 cm. to 1,7 cm. ; of the right ventricle, from 0.4 to 
0.6 cm. 

Generally speaking, the size of the heart corresponds to the size and 
the development of the individual. In judging of an increase or de- 
crease in its size we must consider the weight of the organ and the thick- 
ness of its walls. If the i)erson die while the heart is contracted, the 
walls of the ventricles will appear thicker, their cavities smaller than 
usual. If he die of some exhausting disease like typhoid fever, or if 
decomposition have commenced, the heart walls will usually be flabby 
and the cavities will appear larger than usual. 

Preservation of Specimens. — Parenchymatous and fatty degeneration of the heart 
msiy be studied microscopically by teasing the fresh muscle in one-half-per-cent salt 
solution, or by examining in the same solution fresh sections made with the freezing 
microtome, or by hardening small pieces of the muscle in one-per-cent osmic acid and 
teasing in equal parts of glycerin and water. 

The heart valves may be stretched on a flat cork with pins and hardened in Orth's 
or Zenker's fluid or alcohol. For the methods of detecting bacteria in ulcerative endo- 
carditis, see section on Staining Bacteria. When the presence of bacteria is suspected, 
cultures should be made and the tissues should be preserved in strong alcohol. 

The Pleural Cavities are next examined. The hand is passed into 
each, and the existence of serous or fibrinous exudation or of old adhe- 
sions ascertained. The method of detecting the presence of air has been 

^ Arnold, " Observations on the Weight of the Normal Heart in Adults, in Two 
Hundred and Sixteen Cases. " Reports of the Boston City Hospital, tenth series, 1899, 
page 83. 



THE METHOD OF MAKIXG POST-MOETEM EXAMINATION'S. 25 

given above. After the commencement of putrefaction reddish serum 
may accumulate in the pleural cavities. This should not be mistaken 
for the result of disease. 

The Lungs. — Each lung is lifted up in turn, the vessels, etc., at its base 
are divided, and the organ is removed. If the pleura is very adherent it 
is better to strip off the costal pleura with the lung. After inspecting 
the external surface of the lung, observing its size, shape, color, and con- 
sistence, and the condition of the bronchial lymph nodes, the bronchi 
are opened with scissors having long, narrow, blunt-pointed blades, one 
blade a little longer than the other. The lung is held in the left hand 
with its base upward, the large bronchi which run on the inner side of 
the lower lobe being first opened, afterward those of the ujjper lobe. 
Each bronchus should be followed to its smaller ramifications. 

We should observe the contents of the bronchi and the appearance of 
their walls. In the larger and medium -size bronchi the cartilages in 
their walls do not form complete rings, but appear shining through the 
mucous membrane like irregular white patches. This appearance should 
not be mistaken for a pathological change. In bodies which have been 
dead for some time, especially in cold weather, the bronchial mucous 
membrane may be red and swollen as a post-mortem change. The 
contents of the stomach are sometimes forced, after death, into the 
pharynx, and thence find their way into the trachea and bronchi, giving 
them a peculiar reddish and even gangrenous appearance. Bronchitis 
does not always leave lesions which can be seen after death. The large 
vessels should now be examined for thrombi, emboli, or other lesions. 

After the examination of the bronchi the lung is turned over, the 
vessels, etc. , at its root are grasiDcd with the left hand, and a long, deep in- 
cision is made from apex to base. We observe the appearance and texture 
of the lungs, whether the air vesicles are dilated (emphysematous) or 
filled with serum, blood, or inflammatory exudation. Fluid can be 
pressed out of the air vesicles without breaking down the lung tissue. 
Solid inflammatory exudation, on the other hand, renders the lung more 
resistant and easily broken down. Attention should be paid to the ooz- 
ing of purulent or other fluid from the smaller bronchi when the lung 
is squeezed near the cut surface. It is the rule to find the lower lobes 
more congested than the upper. 

Preservation of the Lungs and Bronchi. — If the lungs have been cut, small 
pieces from the affected portions of lung tissue or bronchi should be hardened in Orth's 
fluid, care being taken not to squeeze or handle them unnecessarily. It is better, when 
the microscopical examination is more important than the macroscopical, not to open the 
lungs at once, but to fill the air spaces with preservative fluid by means of a funnel 
attached to a short rubber tube and canula, which is tied into the main bronchus. In 
this way not only are the minute structures better preserved, but the air vesicles are 
filled out and hardened in an approximately natural condition. Care should be taken 
not to have too great a pressure from the inflowing fluid, since then exudations might 
be displaced or the lung distorted or ruptured. While the lung is being filled it should 
be immersed in a vessel of the same preservative fluid, in which, after closing the can- 
ula or ligating the bronchus, it lies for twenty-four hours. It is then cut into small 
pieces and the hardening completed. A variety of hardening agents may be used: 



26 THE METHOD OF MAKING POST-MOETEM EXAMINATIONS. 

Ortli's fluid or formalin solution (5 : 100) is on the whole the best. If, however, the 
lung is commencing to decay, strong alcohol will stop the process most quickly and 
give as good results as are possible under the circumstances. Alcohol should be used 
when the lungs are to be examined for bacteria. 

It is often desirable, and particularly in cases in which the topography of lesions is 
to be studied, as in acute miliary tuberculosis, acute and chronic phthisis, infarctions, 
etc., to inject the blood-vessels with colored gelatin. The lung should, after the injec- 
tion, be hardened in alcohol. 

The Pharynx, Larynx, (Esophagus, and Thyroid Gland.— For the re- 
moval of these parts the incision through the skin should be carried 
upward as far as practicable— when permissible, to a point one inch be- 
low the chin, the head being allowed to hang backward over the edge of 
the table. 

The soft parts are dissected from the larynx, taking care not to cut 
the thyroid body, and an incision is made through the floor of the 
mouth, following the internal surface of the inferior maxilla. Through 
this incision the fingers are introduced into the mouth, the tongue is drawn 
down, the i30Sterior wall of the pharynx is divided above the tonsils, and 
the tongue, pharynx, and larynx are drawn out together. These organs 
are then pulled downward, and with the aid of the knife the trachea and 
oesophagus are removed entire, the oesophagus being cut just above the 
stomach. If the contents of the stomach are to be preserved, as in cases 
of suspected poisoning, a ligature is put around the oesophagus just be- 
low the point at which it is to be cut off. 

With the enterotome the pharynx and oesophagus are now slit open 
upon their posterior surfaces. The mucous membrane thus exposed is 
examined for evidences of caustic poisons, of inflammation, tumors, 
strictures, varices, etc. The enterotome is next introduced into the 
larynx, and this organ and the trachea are laid open along the posterior 
wall. Here we look for oedema of the aryteno-epiglottidean folds 
(oedema of the glottis), for evidences of catarrhal, croupous, ulcerative, 
and syphilitic inflammation, and for tumors and lesions of the laryngeal 
cartilages. CEdema and redness of the larynx may result from post-mor- 
tem changes, especially in bodies which have been kept for several days 
in cold weather. A well-marked oedema glottidis during life may leave 
no trace after death. Putrefactive changes usually commence early in 
the larynx and trachea. 

The thyroid gland is dissected off and examined. Its weight varies 
considerably, being, according to Krause, somewhat over 30 grams. 

Preservation of the Pharynx, Larynx, Trachea, etc. — These structures are 
freed from superfluous tissue and suspended entire by a thread in a large quantity of 
Ortli's fluid or Flemming's osmic-acid mixture, after which the hardening is completed 
in the usual w^ay. The oesophagus should be stretched loosely on sheet cork with pins, 
and hardened in either of the above fluids. The thyroid may be cut into small pieces 
and similarly hardened. 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 27 



The Abdomen. 

Eeturning now to the abdomiual cavity, we first dissect off the omen- 
tum. Tubercles of the peritoneum may be best seen in the omentum. 
The colon is then raised and dissected free, to the csecum on one side and 
to the rectum on the other. The colon and small intestines are then 
drawn first to the right and then to the left side, so as to exi30se in turn 
the right and left kidneys. As each kidney is brought into view an in- 
cision is made through the peritoneum over the track of the ureter. The 
ureter is followed through its entire length and its condition ascertained. 

Sometimes one, more rarely all, of the abdominal viscera are unusually 
movable, owing to a relaxation of their ligamentous or other supi)orts. 
This condition — enteroptosis — is uncommon in the liver, more frequent 
in the spleen, and especially so in the kidneys. It has been occasionally 
described in the stomach and intestines. 

The Kidneys. — These organs are now removed, the peritoneum and 
fat being separated from them with the hand, and the vessels being di- 
vided with the knife. The adrenals, at the upper end of each kidney, 
are removed at the same time. The kidneys may be softened by putre- 
faction, or the surface may have a greenish-gray color, caused by the 
post-mortem action of putrefactive gases on the haemoglobin. 

An incision is made through the capsule, along the convex border of 
the kidney, and the membrane stripped off. We notice the degree of 
adherence of the capsule to the kidney, and also the surface of the latter, 
whether smooth or roughened, pale, congested, or mottled ; an incision 
is made along the convex surface down to the pelvis, so that the organ 
is divided into halves. We observe the relative thickness of the cortical 
and pyramidal portions, as well as the size of the entire organ. To as- 
certain the latter point, it is well to weigh each kidney; the normal 
weight is from 130 to 150 grams. The left kidney is, according to Orth, 
from 5 to 7 grams heavier than the right. At from twenty to thirtj -five 
years of age, according to Thoma, the weight of the heart is to the 
weight of both kidneys as 1 : 1.1. The weight of the kidneys of adults is 
given by Tierordt in general as about 0.18 per cent of that of the entire 
body. 

It is necessary to remember that in a kidney which is much atrophied 
there may be an increase of fat in the pelvis, which gives the organ 
nearly its normal size and weight, while the kidney tissue proper may 
have in great measure disappeared. 

We now inspect the kidney tissue more closely, especially the cortical 
portion. The pyramids consist largely of tubes running in nearly 
straight lines from the apex to the base of each pyramid. These straight 
tubes pass from the pyramids into the cortex in bundles, called medul- 
lary rays, many of them retaining their straight course until they nearly 
reach the surface of the kidney. These straight tubules send off branches 
on all sides of the rays, which become convoluted, form Heule's loops. 



28 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

and finally terminate in the glomernli or Malpighian bodies. In this 
way the cortex of the kidney, as seen in section, is divided into alternate 
bands of straight tnbes, and convoluted tubes, with glomeruli ; both sets 
of bands being perpendicular to the surface of the kidney, and called re- 
spectively medullary rays and labyrinths. About the convoluted tubules 
and glomeruli is a rich venous plexus ; and since after death the blood 
usually remains in this plexus and in the glomeruli, the bands containing 
the convoluted tubules, i. e. , the labyrinths, usually appear red, while the 
medullary rays are grayish -white. In a normal kidney, therefore, the 
cortex should be regularly striped in narrow alternating red and whitish 
bands. 

The average thickness of the cortex of the kidney is from 4 to G mm. 

If there be extensive congestion, the entire cortex is red. If the epi- 
thelium of the tubules degenerates and fills them up, or if there are con- 
siderable changes in the interstitial tissue, the regular bands are lost and 
the cortex is irregularly mottled. If the tubular epithelium becomes 
filled with fat globules, this is indicated by an opaque yellow color of the 
affected parts ; in many cases, therefore, the existence of kidney lesion 
can be recognized with the naked eye. 

If waxy degeneration be present to a marked extent, it may be mani- 
fest by a peculiar translucent appearance of the affected parts, but in 
most cases it is necessary to aiDply reagents to demonstrate it satisfac- 
torily. The cut surface of the kidney is washed with water, to free it 
from blood, and repeatedly brushed with an aqueous solution of iodine 
(iodine 1 part, potassium iodide 3 parts, water 100 parts). The glo- 
meruli and the blood-vessels are most frequently affected, and, if so, they 
may appear as mahogany -colored dots and lines on a yellow ground. 

But this reaction is not constant, and for accurate detection of amyl- 
oid substance, recourse should be had to other reagents applied to sec- 
tions of the hardened tissues (see page 83). 

The pelvis of the kidney should be examined for inflammatory lesions 
and calculi. Sometimes a whitish fluid is seen in the pelvis and can be 
squeezed from the j)apill8e ; this is produced by a post-mortem desqua- 
mation of the epithelium, but is likely to be mistaken for pus. 

Preservation of the Kidney. — If the kidney be not opened, the blood-vessels 
may be injected through the renal artery, slowly and under a low pressure, with Orth's 
fluid or Flemming's osmic-acid mixture. After the vessels are filled with either of the 
above fluids the former are tied, and the entire organ is placed in a large quantity of the 
injecting fluid for twenty-four hours. Tlie kidney is then cut into small pieces, and 
the hardening is completed in the usual way. 

In most cases, however, tlie kidneys will have been opened for inspection at the 
autopsy. Then small pieces are removed from the various regions and hardened in the 
above fluids. 

Kidneys which are to be examined for the presence of bacteria should be cut into 
small pieces and placed at once in strong alcohol, which should be changed once or 
twice, and in which they are permanently preserved. 

The Adrenals — Suprarenal Capsules. — These are, in the foetus, of an 
ovoidal ; in the adult, of a triangular shape. They are situated at the 



THE METHOD OF MAKING POST-MOETEM EXAMIK^ATIOXS. 29 

upper and inner border of the kidney, to ^ hich they are loosely attached 
by connective tissue. On the anterior surface is an irregular fissure, 
called the hilus, from which the veins emerge. The size of the adrenals 
varies considerably, but in the adult the average vertical diameter is from 
3.2 cm. to 4.5 cm., the transverse diameter about 3.2 cm., and they are 
from 4.2 mm. to 6.4 mm. in thickness. They weigh in the adult 4 to 8 
grams. They are relatively larger in children than in adults. They are 
composed of a cortical and a medullary i)ortion, the cortex forming a yel- 
lowish sliell around the dark-red or brown medulla. They are enclosed 
in a connective -tissue capsule, from which fibrous processes extend in- 
ward, dividing the gland into a series of irregular chambers. Those in 
the cortex are mostly elongated, giving this portion a striated appear- 
ance, while those in the medulla are i^olyhedral. It is in these spaces 
that the i^arenchyma cells lie. The adrenals readily decompose; the 
inner layer of the cortex may soften and break down, so that the outer 
zone forms a sort of cyst filled with reddish-brown broken-down sub- 
stance. Hypertrophy, tuberculosis, and cheesy degeneration, fatty de- 
generation, and tumors are to be looked for. 

Preservation. — The adrenals should be hardened in Orth's fluid, or in strong 
alcohol. 

The Spleen. — This organ has, when removed from the body, the gen- 
eral shape of a flattened ellipsoid, most curved on its external and pos- 
terior surface. It is situated in an oblique position on the left side of 
the stomach, and between its cardiac end and the diaphragm. The 
vessels are given off from its inner surface, which is crossed by a more 
or less well-marked vertical ridge. The point of emergence of the ves- 
sels is called the hilus. Its long diameter extends from the seventh inter- 
costal space to the eleventh rib. Its upper portion is separated from the 
ribs by the lungs ; its lower portion by the diaj)hragm. 

It is, according to Yierordt, on the average, from 12 to 13 cm. long ; 
from 7 to 8 cm. broad, and about 3 cm. thick. Its average weight is 
about 171 grams. The dimensions of the spleen as given by Krause are 
somewhat greater than the above. But its measurement and weight 
vary considerably within the limits of health. It is in these respects 
the most variable organ in the body. In old age the average weight 
gradually diminishes. 

The spleen is enclosed in a fibrous capsule covered with peritoneum. 
The parenchyma is formed of blood-vessels and fibrillar connective tissue, 
and of a soft, dark-red pulp in which are embedded whitish spheroidal 
or elongated bodies, the glomeruli, or Malpighian bodies. In the normal 
human spleen the glomeruli are usually hardly perceptible to the naked 
eye, but sometimes they are very plain. Sometimes the fibrous stroma 
is very apparent, sometimes not. 

The size, consistence, and color of the organ vary a good deal within 
normal limits; it may soften in decomposition. Thickenings of the cap- 
sule and abnormal adhesions are very common, and often occur without 



30 THE METHOD OP MAKING POST-MORTEM EXAMINATIONS. 

any clinical history indicating disease. We should look for changes in 
size, color, and hardness ; for pigmentation, hyperplasia of the connec- 
tive tissue, amyloid degeneration, tubercles, and infarctions. 

IS'ot infrequently one or more spheroidal or flattened so-called acces- 
sory spleens are found in the vicinity of the spleen ; they vary in size 
from that of a pea to that of a walnut. 

Preservation. — In certain diseases of the pulp, leukaemia, leucocythaemia, etc., the 
tissue should be teased, Avlien fresh, in one-half-per-cent salt solution, or examined by 
the staining methods described under the lesions of the blood. For general purposes 
small pieces of the organ are hardened in Orth's fluid, Flemming's osmic-acid mixture, 
or in alcohol. 

The Intestines. — The rectum is divided, the intestine seized with the 
left hand, and, being kept stretched, is separated from its attachments 
by repeated incisions through the mesentery close to the gut, until the 
duodenum is reached, where the intestine is again cut off. The opera- 
tion is more cleanly if, before dividing the gut, ligatures are placed 
around it at either end. The entire length of the gut is now laid open 
with the enter otome along the mesenteric attachment, the mucous mem- 
brane is cleaned with a stream of water and then examined. 

In cases of suspected poisoning, a ligature should be placed around 
the rectal end of the gut and two around the duodenal end, and it should 
then be cut off below the former and between the latter ligatures. The 
gut is now opened and the contents are emptied into a clean glass jar for 
delivery to the chemist, care being taken that they be not allowed to 
touch anything but the inner surface of the jar. After washing the in- 
testine in pure, fresh water and examining it, it should be placed entire 
in another clean jar and the jar sealed. 

Cadaveric lividities are very common in the intestines, and are 
usually most marked in the dependent portions. They are apt to occur 
in patches, but may be diffuse and very extensive. If the wall of the 
gut be stretched, they are often seen to be discontinuous, owing to the 
pressure of the blood from the parts which are squeezed by folds. Small 
patches of arborescent or diffuse red staining are often seen, formed by 
the imbibition from the vessels of decomposing haemoglobin. In the 
more advanced stages of decomposition the mucosa may be softened and 
loosened. A dark purple or brownish discoloration of the entire intes- 
tinal wall is frequently seen, either diffuse or in patches. Much experi- 
ence and careful observation are requisite in forming a correct judgment 
regarding the significance of changes of color in the intestines. Caution 
is necessary in distinguishing normal digestive hypersemia from abnor- 
mal congestion. A very considerable congestion may exist without 
disease. 

The lesions ordinarily to be looked for are catarrhal, croupous, and 
ulcerative inflammations, perforations, haemorrhages, strictures, tumors, 
amyloid degeneration, swelling and ulceration of the solitary follicles 
and Peyer's patches, and pigmentation. For the detection of amyloid 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 31 

degeneration of the mucosa this structure should be carefully washed 
and brushed with a solution of iodine (see p. 28). 

Preservation. — For the general purposes of microscopic study, portions of the gut 
should be gently stretched on cork (the mucosa side free) and hardened in Orth's fluid 
or in Flemming's osmic-acid mixture. 

For obvious reasons the mucous membrane should be handled as little as possible, 
for, in the majority of cases, decomposition and softening have already set in at the 
time of the autopsy, and, under the most favorable conditions, the epithelium is very 
easily rubbed off. 

In cases in which the most perfect preservation of the topographical features, as 
well as the minute structure of the intestinal mucosa, is desired, even at the expense of 
an inspection of the fresh tissue, another mode of procedure is to be recommended. 
Selected segments of the gut are, after removal from the body, allowed to remain un- 
opened on the table while ligatures are tied around the ends. The isolated segments, 
or the whole gut, are now to be moderately filled — not distended — with one of the 
above fluids b}' means of a syringe with a needle canula ; or one end of the segment 
may be tied and the fixative introduced through a funnel at the other, which end is then 
ligated. The segments to be preserved should now be placed unopened in the fixative 
solution. After twenty -four hours they may be opened with scissors or a sharp knife, 
cut into suitable pieces, and kept permanently in eighty-per-cent alcohol. 

The Stomach and Duodenum. — We now introduce the enterotome into 
the duodenum at its transverse portion, and open it on the convex border. 

When the pylorus is reached the incision is carried obliquely over to 
the greater curvature of the stomach, along which it is extended as far as 
the oesophageal opening, and the organ examined in situ ; or, if a more 
careful examination of the stomach is called for, after ascertaining 
whether or not the bile duct is pervious (see below), the duodenum and 
stomach may be removed together, and the stomach opened and examined 
on the table. Alterations in size and form, the presence of tumors, 
ulcers, etc. , may now be sought for. 

If poisoning be suspected, a ligature should have been placed, earlier 
in the examination (see above), around the lower end of the oesophagus 
and the duodenum. The stomach and duodenum are now removed to- 
gether unopened. They are to be opened in a carefully cleansed glass 
jar, and after an inspection of the mucous membrane and the contents 
with the naked eje and a hand lens, stomach, duodenum, and contents 
are to be sealed in the jar for the chemist. 

We now look for the orifice of the bile duct, which will be found 
about the middle of the descending portion of the duodenum on its con- 
cave border. Pressure on the gall bladder or on the common duct will 
usually cause the bile to flow into the intestine if the ducts are pervious. 
But a sufficient degree of stoppage may exist in the ducts to give rise to 
marked symptoms of disease, without preventing the flow of bile under 
these conditions, even with a moderate pressure. A long director is now 
passed into the gall duct, which is laid completely open; ulcerations, 
cicatrices, gall stones, inflammatory lesions, and tumors are looked for. 
In stricture of the gall duct the mucous membrane above will often be 
found bile-stained, while below it is colorless. At this point, should 



32 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

there be any special reason for doing so, the portal vein, which lies close 
behind the ductns choledochus, should be opened and examined for peri- 
phlebitis, phlebitis, and thrombosis. The mucous membranes of the 
duodenum and stomach are now examined. Acute inflammation from 
caustic poisons, chronic catarrhal inflammations, haemorrhages, ulcers, 
erosions, swelling of the solitary follicles (lymph nodules), and tumors 
are lesions most frequently seen. We sometimes find a diffuse congestion 
of the stomach, similar to that produced by irritant poisons, as a result 
of doses of croton oil given just before death. 

Preservation. — The same methods should be used as for the intestines (see above). 
Tumors should be cut into small pieces and hardened in Orth's fluid or five-per-cent 
formalin. 

The Liver, ^To remove the liver, the diaphragm is first divided on 
one side of the suspensory ligament as far back as the spine ; the suspen- 
sory ligament is then divided ; then the right and left lobes being in turn 
raised, the lateral ligaments are severed. Then, the left lobe being seized, 
the organ is dragged obliquely downward into the abdominal cavity, the 
remaining attachments being dissected away. The liver is first laid on 
its superior surface and the gall bladder and its contents are examined. 
The character of the gall is to be determined, and gall stones, inflam- 
matory lesions, and tumors are to be sought for. To determine the 
actual size of the organ, it should be both measured and weighed. Its 
size varies greatly in different healthy individuals, but in general it may 
be said that it measures from 25 to 30 cm. transversely, from 15.3 to 18 
cm. antero-posteriorly, and from 9 to 12 cm. at its thickest part ; its or- 
dinary weight is between 1,550 and 1,860 grams. In children its weight 
relative to that of the body is greater than in adults. The liver is 
increased in size and weight during digestion and by congestion from 
any cause. 

The convex surface of the right lobe of the liver not infrequently 
shows several grooves running from front to back, approximately par- 
allel with the suspensory ligament of the liver. These grooves, which 
may be found in persons of all ages, are believed by some to be usually 
congenital, by others to be the result of pressure of the diaphragm and 
the abdominal muscles on a relaxed atrophic liver. They seem in any 
event to be of no practical importance. On the other hand, a transverse 
groove running at right angles to the axis of the body is a not infrequent 
result of tight lacing, and is usually associated with local connective- 
tissue thickening of the capsule and underlying tissue of the liver. In 
this way the liver may become much distorted and the gall bladder com- 
promised. 

The capsule of the liver is now examined ; the organ is then laid on its 
lower surface and several deep incisions are made from above downward. 
The color and consistence of the liver tissue should be noticed, also the 
distinctness with which the lobular outlines can be seen ; whether or not 
the centres of the lobules are congested or their peripheries lighter in 
color than usual ; the presence of tumors, tubercles, abscess, ecchinococ- 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 33 

cus, new connective tissue, and pigmentation. Suspected amyloid de- 
generation should be tested for by iodine solution. 

We often find the surface of the liver of a greenish or very dark- 
brown color ; less frequently the same color extends into the substance of 
the organ. This discoloration, which is entirely post mortem, is, like 
the similar discoloration of other internal organs, produced by the action 
of the gases of putrefaction on the coloring matter of the blood. 

Preservation. — For the study of parenchj-matous degeneration, sections of the 
fresh frozen tissue or small teased fragments should be examined in half-per-cent salt 
solution. For general purposes small pieces should be hardened in Orth's fluid or in 
formalin solution (5 : 100) or in alcohol. Tumors should be treated in the same way. 

The Pancreas. — This organ, of a light yellowish-red color, is elon- 
gated, irregularly prismatic in shape, and flattened antero-posteriorly ; 
the right end, called the head, is broader than the rest and lies in the 
concavity of the duodenum. The remainder of the organ, the body and 
tail, are usually taj)ering and lie transversely in the abdominal cavity, 
the tail reaching to the spleen. Its size and weight vary considerably ; 
its usual length is from 15.3 to 23 cm. ; its breadth about 3.8 to 45 cm. ; its 
thickness about 1.3 to 3.8 cm. ; its weight is usually from 70 to 108 grams. 
The organ may be rounded instead of flattened ; the head and tail may 
be disproiDortionately large ; the tail may be unusually long or may be 
divided or curved. The superior mesenteric artery and vein, which pass 
behind the gland, are usually partly embedded in it, but are sometimes 
completely enclosed. 

A longitudinal incision should be made through the whole gland, 
and its substance and duct should be searched for calculi, tumors, mal- 
formations, and evidences of acute and chronic inflammation, fat necro- 
sis, and amyloid degeneration of the blood-vessels. The pancreas is 
frequently of a dark-red color from post-mortem staining. 

Preservation. — Portions of this organ should be hardened in strong alcohol, 
Orth's fluid, or in Flemming's osmic-acid mixture. 

The examination of the thoracic duct, which lies to the right and 
posterior to the aorta, may now be made. Among the most important 
of its lesions is tuberculosis, since it has been shown that from a tuber- 
culous lesion here the generalization of the bacilli not infrequently oc- 
curs. Inflammatory lesions, carcinoma, partial or total occlusion from 
pressure may be found. 

The solar plexus, which surrounds the origin of the coeliac axis and 
the superior mesenteric artery and lies between the adrenals, may now 
be sought. Lesions of the semilunar and other ganglia are to be noted — 
atrophy, pigmentation, and degenerations. 

The ganglia may be fixed and hardened in Orth's fluid or in the osmic-acid 
mixture. 

The Aorta. — This vessel either in situ or after removal should be 
opened by an incision extending its whole length and continued into its 
larger branches. 
3 



34 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 



The Genito-Ueinaey Organs. 

The Male Organs. — If the urine is to be examined it may be drawn off 
with a catheter; or a vertical incision may be made into the bladder just 
above the symphysis pubis, and some of the urine dipped out. The cut 
end of the rectum should now be grasped with the left hand and raised 
up, and this and the bladder, prostate gland, etc., dissected away from 
the pelvis, the knife being carried close to the bone. The bladder is 
now drawn backward and the loose tissue close under the symphysis 
pubis cut. The body of the penis is then shoved backward within the 
skin and dissected away from behind, beneath the symphysis, and finally 
cut off just behind the gians penis. The penis and bladder are now 
drawn backward and upward, and the pelvic organs removed together. 
Or, the iDcnis may be removed by sawing away the bones above the pubic 
arch, and then dissecting away the penis, whose root is thus exposed. 

The pelvic organs are then laid on the table, the bladder uppermost ; 
a long director is passed into the urethra, which is opened on its upper 
surface through its entire length, and the bladder widely opened. In 
the urethra the presence of strictures, diverticula, ulcers, inflammatory 
lesions, is to be noticed ; in the Madder inflammatory lesions, hypertro- 
phies, congestion and ecchymosis of the mucous membrane, hyperplasia 
and ulcers of the lymph nodules, and tumors. The organs are now 
turned over ; the rectum is opened and examined for varicose veins, haem- 
orrhages, ulcers, strictures, and tumors. The prostate gland is then cut 
into and the presence of calculi, inflammatory lesions, hypertrophies, 
and tumors sought for. Lastly, the vesicidce seminaJes are examined, in 
which, though rarely, we may find evidences of tuberculous inflammation 
and dilatation. 

TJie Testicles may be removed, when necessary, without cutting the 
scrotum, by enlarging the inguinal canals from within and crowding the 
glands through them and cutting them off. The average weight of the 
adult testicle with its epididymis is, according to Krause, from 15 to 
24.5 grams. Inflammatory lesions, tuberculosis, abscesses, and tumors 
are the most frequent lesions. 

Preservation. — The urethral canal and bladder maybe pinned open and hardened 
in Orth's fluid or in Flemraing's osmic-acid mixture. The prostate, vesiculse seminales, 
testicles, and tumors may be hardened in the same fluids. 

The Female Organs. — The position and general condition of the pelvic 
organs should first be determined by inspection. Abnormal adhesions 
of the ovaries, broad ligaments, Fallopian tubes, and uterus ; malposi- 
tions of the uterus ; subserous tumors of the uterus, and ovarian tumors, 
are frequently observed. Haemorrhage into the posterior cul-de-sac is 
sometimes found. The urine should be collected, if necessary, as above 
directed ; the organs should be dissected away laterally, as in the male, 
care being taken not to injure the ovaries and Fallopian tubes. The 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 35 

bladder is then drawn strongly backward and upward, and dissected 
away from the symphysis and the pubic arch, and, the point of the knife 
being carried forward and downward, the vagina is cut off in its lower 
third, the rectum severed just above the anus, the remaining attachments 
cut, and the pelvic organs are taken out together. If it be necessary to 
remove the external generative organs, after freeing the lateral surfaces 
of the internal organs and the bladder, the legs are widely separated and 
the vulva and anus circumscribed by a deep incision. The tissues close 
beneath the pubic arch are now dissected away from below, and the 
vulva is thrust back beneath the symphysis ; it is now seized above the 
bone, and together with the anus dissected away and removed with the 
other organs. 

The bladder is first opened and examined. The vulva may now be 
examined for hypertrophies, inflammatory lesions, ulcers, cicatrices, 
cysts, and tumors. The vagina is opened along the anterior surface ; its 
more common lesions are inflammations, fistulse, ulcers, tumors, and 
rarely cysts. 

The Uterus. — Before opening this organ its size and shape should be 
determined. The adult virgin uterus is a pear-shaped body, flattened 
antero -posteriorly ; the upper portion, or body, is directed upward and 
forward, while the lower portion, the cervix, is directed downward and 
backward. It is covered anteriorly by peritoneum to a point a little 
below the level of the os internum; posteriorly, to a point a little below 
the level of its junction with the vagina. The iDcritoneal investment 
separates from the organ at the sides to form the broad ligaments. The 
uterus is held in position by the broad and round ligaments and by its 
attachments to the bladder and rectum and vagina. The upper end, 
the fundus, does not extend above the level of the brim of the pelvis. 
Its average length is about 7.6 cm.; its breadth about 5.1 cm.; its 
thickness about 2.5 cm. ; its average weight is about 31 to 46 grams. 
During menstruation the uterus is slightly enlarged, the mucous mem- 
branes of the body becomes thicker, softer, and its vessels are engorged 
with blood ; while its inner surface is more or less thickly covered with 
blood and cell detritus. A description of the complicated changes in the 
uterus which i)regnancy entails may be found in the woi'ks on obstetrics. 
After pregnancy the uterus does not return to its original size, but re- 
mains somewhat larger ; the os is wider and frequently flssured. 

We not infrequently find in the mucous membrane of the lower i)art 
of the cervix small transparent, spheroidal structures, called ovula 
Kabothi ; these are small retention cysts caused by the closure of the 
orifices of the mucous glands. The more common lesions observed in 
the uterus are malpositions, malformations, lacerations, ulcerations of 
the cervix, acute and chronic inflammation of the mucous membrane or 
muscularis, or both, thrombosis and inflammation of the veins, and 
tumors. 

In the infant the uterus is small, the body flattened, the cervix dis- 
proportionately large. During childhood the organ increases in size, 



36 THE METHOD OF MAKING POST-MOKTEM EXAMINATIONS. 

but the body remains small in proportion to the cervix. At puberty, the 
shape changes, and the body becomes larger. 

The Ovaries are flattened, ovoidal bodies, situated one on each side, 
and lying nearly horizontally at the back of the broad ligament of the 
uterus. Their size is variable, and they are usually largest in the virgin 
state. They measure about 3.8 cm. in length, 1.9 cm. in breadth, and 
nearly 1.3 cm. in thickness. Their average weight is from 3.9 to 6.5 
grams. The sides of the ovary and its posterior border are free ; it is 
attached along the anterior border ; to its end is attached the ovarian 
ligament; to its outer extremity one of the fimbriae of the Fallopian tube. 
The ovary is covered on its free surface by cylindrical epithelium, and 
its surface is less glistening than the general peritoneum. The surface 
of the ovary is smooth in the young, but become rougher and depressed 
in spots as the process of ovulation goes on. In adult females we 
usually find corpora lutea in their various stages. We should seek for 
evidences of acute and chronic inflammation, for tumors and cysts. 

Tlie Fallojnan Tubes, lying in the upper margin of the broad liga- 
ments, are from 7.6 to 10 cm. in length. The length often differs con- 
siderably on the two sides. They commence at the upper angles of the 
uterus as small perforated cords, which become larger further outward 
and bend backward and downward toward the ovary. They terminate 
in an expanded fimbriated extremity about 2.5 cm. beyond the ovary. 
They are covered by peritoneum, and the mucous membrane lining them, 
continuous with that of the uterus, is thrown into longitudinal folds. 
Malpositions by adhesions, closure, inflammations, and cysts are the 
more common lesions. The possibility of tubal pregnancy should be 
borne in mind. 

Preservation. — All of these organs and their tumors may be hardened in Ortli's 
fluid, or in Flemming's osmic-acid mixture. The vagina should be stretched flat on cork, 
and the cavitj^ of the uterus laid wide open. Great care should be taken not to touch 
either the internal surface of the uterus or the external surfaces of the ovaries, since 
in both the epithelium is very easily rubbed off. 

It is better, after opening them by a transverse incision, to suspend the ovaries by 
a thread in a jar of the preservative fluid than to let them lie on the bottom, since the 
epithelium is thus less likely to be rubbed off. Larger cysts of the ovary for exhibition 
purposes should be distended with preservative fluid (see page 61). 

The Closure of the Body after the Post-Mortem 
Examination. 

At the end of the autopsy the body should be restored as nearly as 
possible to its natural external appearance. 

Fluids should be removed, vacant spaces filled with absorbent mate- 
rial, such as cotton, jute, or sawdust, and the incisions closed by sutures. 



THE METHOD OF MAKING POST -MORTEM EXAMINATIONS. 37 



Bacterial Examination of Post-Mortem Specimens. 

It is often important to make a thorough post-mortem examination 
by cultures as well as morphologically of the blood and of all the vis- 
cera. This is important not only in those cases which during life gave 
clinical evidence of general infection, but also in many forms of disease 
whose nature is still wholly obscure. 

In the interpretation of the results of all such examinations, however, 
it should be borne in mind that after death a new distribution of germs 
may occur, and that from the gastro- intestinal canal and from other sur- 
faces or cavities of the body micro-organisms may, as decomposition 
progresses, penetrate the tissues and the viscera. 

A careful consideration of the general conditions under which the 
body has been kept and its state of decomposition is of especial impor- 
tance in the interpretation of the significance of the Bacillus coli com- 
munis, which is always present in such enormous numbers in the intes- 
tinal canal, and which is not only apt to effect wide distribution in the 
body after death, but as a result of careless manipulation is likely to be 
accidentally brought in contact with other viscera after the opening of 
the gut. The preparation of cover slips for staining and the making of 
cultures is, as a rule, best done at the autoi)sy table. 

It is well as each organ is exposed — commencing with the heart — to 
sear the surface of the organ to be examined with a broad-bladed knife 
heated over a flame, and then, making an incision through the seared 
surface with a sterilized scalpel, to press a sterilized cotton swab (see 
p. 155) into the opening and absorb the juices which exude, or to pick 
out a small fragment of the solid tissue from the depths of the opening, 
or to secure some of the blood or fluid on a sterilized platinum loop ; 
and then with the material thus procured make the required cultures 
and afterward the cover-slip smears for staining. 

If it be necessary to transport the material to the laboratory before 
making cultures, it is well to reserve the unopened organs, or large por- 
tions of these in the case of the solid viscera, and to wrap each separately 
in a cloth saturated with sublimate solution, or to put each in a separate 
sterile receptacle for transportation. 

It is well to remember that in the last hours of life the safeguards 
of the body against the entrance and growth of micro-organisms may 
be ineffective, so that the determination of the significance of bacteria 
in the tissues a short time after death requires care and experience. ' 

Autopsies in Medico-Legal Cases. 

While every autopsy should be made as carefully and completely 
as circumstances permit, it should be always borne in mind that in 
examinations which may have medico -legal bearings it is of the highest 

^ For details of bacterial flora of the Immau body, with bibl., see page 159. 



38 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

importance to examine thoronghly both macroscopically and microscop- 
ically every part of the body from which light may be derived as to the 
cause of death, for in medico-legal cases it is not infrequently as impor- 
tant to be able by a complete examination to declare the absence of le- 
sions which could cause death as to determine the presence of those upon 
which the opinion as to the actual cause of death in a particular case 
rests. Bearing this in mind, the technique of autopsy-making is essen- 
tially the same whatever the ends which the facts elicited may be des- 
tined to serve. 

Autopsies in Cases of Suspected Poisoning. 

In cases of suspected poisoning which may possibly have a medico- 
legal bearing, the examination should be made with extreme care and 
thoroughness. The inspection of the body and the examination of all 
the viscera should be thorough and detailed. Every appearance should 
be noted at the time, and nothing left to the memory. It is well to have 
an assistant record the observations as they are made. The disposition 
of the parts and organs in jars should also be noted at the same time. 

It is important to remember that many i^oisons destroy life without 
producing appreciable lesions, and also that many cases of sudden death 
occur, not due to poisons, and without any discoverable cause. 

In bodies which are exhumed for examination, the tissues may be so 
changed by decomposition that it is impossible to say whether lesions 
have or have not existed. In such cases the careful and separate preser- 
vation of the viscera and other i^arts for chemical examination, is often 
all that can be done. 

It is always best, in cases of suspected iDoisoning, to preserve for the 
chemist not only the stomach and intestines, but the entire liver and 
brain ; or, if only portions of these can be saved, these portions should 
be carefully weighed, as well as the entire organs, and the relative 
amount of tissue reserved carefully noted at the time. It is even well, 
particularly in cases in which the administration of the readily diffusible 
poisons, such as arsenic, strychnia, etc., is suspected, to preserve the 
whole of all the internal organs, together with a large piece of muscle 
and bone ; since with large quantities of tissue the results of the chemi- 
cal analysis depend less upon calculations, and are hence more compre- 
hensible to the average jury. In all such cases jars should, if possible, 
be procured which have never been used before, and these should be 
carefully washed and rinsed with distilled water. They should have 
glass stoppers and be sealed at once and carefully labelled before leaving 
the hands of the operator. If they can be delivered to the chemist with- 
out much delay, no preservative fluid should be added. If they are to 
be kept for a considerable time, pending the action of a coroner's jury 
or for some other reason, a small quantity of pure strong alcohol may 
be poured over them. In this case the operator should be particular to 
preserve a quantity, at least half a pint, of the specimen of alcohol used. 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 39 

in a clean, sealed, and labelled bottle, so that this may be tested by the 
chemist and be proven to be free from the poison. It is better in all 
cases, howe^^er, to avoid, if possible, the nse of alcohol. In all antop- 
sies which may have medico -legal importance full notes should be taken 
by an assistant as the operation proceeds, carefully read over immediately 
afterward and dated, and kept by the operator for future reference. 
The labelling and disposition of the jars should be recorded in the notes. 
The specimens should not for a moment be out of the sight of the o^Der- 
ator until they are placed under lock and key and seal, or are delivered 
to some authorized person, so that there may be no question of their 
identity should the case come into court. 

Examination of the Bodies of New-born Children. 

In examining the bodies of new-born cliildren, we may have to determine, besides 
the ordinary lesions of disease, the age of the child, whether it was born alive, how long 
it has been dead, what was the cause of death. 

The Size, Age, and General Chakacters of the Fcetus. — Caspar^ gives the fol- 
lowing description of the foetus during the different months of intrauterine life: 

At the fourth week the embryo is 8 to 13 mm. long. The cleft of the mouth and 
two points indicating the eyes can be recognized in the head. The extremities are rep- 
resented by little w^art-like projections. The heart can be distinguished; the liver is 
disproportionately large. The umbilical vessels are not yet formed. The entire ovum 
has about the size of a walnut. 

At the eighth loeek the embryo is 3.3 to 4 cm. long. The head forms more than a 
third of the entire body ; the mouth is very large ; the nose and lips can be distin- 
guished, but not the external ear. The hand is longer than the forearm ; the fingers 
are formed, but joined together; the toes look like little buds; the soles of the feet are 
turned inward. The position of the anus is indicated by a point. The abdomen is 
closed. All the viscera can be recognized. Centres of ossification are formed in the 
apophysis of the first cervical vertebra, the humerus, radius, scapula, ribs, and cranial 
bones. There are rudimentary external genitals, but the sex can hardly be distin- 
guished. The ovum has about the size of a hen's egg. 

At the twelfth iceek the placenta is formed. The embryo is 5 to 6.5 cm. long and 
weighs about 31 grams. The head is separated from the thorax by a distinct neck. The 
eyes and mouth are closed. The nails can be perceived on the fingers. The sex can be 
recognized. The umbilical cord is inserted near the pubes; the muscles begin to be 
recognizable. The thymus and adrenals are formed. The cerebrum, cerebellum, me- 
dulla, and the cavities of the heart can be recognized. The humerus is 1.7 mm. long; 
the radius 5.5 mm. ; the ulna 6.6 mm. ; the femur and tibia 4.4 to 6.6 mm. ; the fibula 
0.5 mm. The ovum is as large as a goose's egg. 

At the sixteenth iceek the embryo is 13 to 15 cm. long and weighs 77 to 93 grams. 
The skin is of a rose-red color, and has considerable consistence. The formation of fat 
in the subcutaneous tissue has begun. The scrotum and labia are formed. The face 
begins to assume its characteristic appearance. There is whitish meconium in the duo- 
denum. The liver is not so disproportionately large, and the gall bladder is formed ; 
the anus is open. The length of the humerus, radius, and ulna is 1.7 cm. ; the femur 
and tibia, 8.8 to 11 cm. The calcaneus begins to ossify at the middle of the fourth 
month. 

At the twentieth week the embryo is 26 to 28 cm. long; it weighs from 225 to 320 
grams. The nails are quite perceptible. There is a thin down on the head. The head 
is still disproportionately large, occupying about one- fourth of the body. There is as 
yet none of the vernix caseosa. The secretion of bile has commenced and stains the 

^Caspar, "Handbook of Forensic Medicine. " Revised German Edition by Liman, 
or Sydenham Society Translation. 



40 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

meconium. The insertion of the umbilical cord is still further off from the pubes. The 
liver, heart, and kidneys are large in proportion to the other organs. The convolutions 
of the brain cannot be recognized. The humerus is 2.8 to 3 cm. long; the radius 2.6 
cm. ; the ulna 2.8 cm. ; the femur, tibia, and fibula, each 2.6 cm. The astragalus and 
the upper part of the sternum begin to ossify. 

From this time on the length of the foetus forms an approximately accurate basis 
for the estunation of its age. From this period till its maturity one-fifth of the length of 
thefcetiis, determined in centimetres, nearly corresponds to the number of months of its age. 
From this time on the weight exhibits marked individual differences, and is therefore a 
less reliable criterion of its age than is the length. 

At the ticenty -fourth 'week the embryo is 31 to 34 cm. long and weighs 750 to 875 
grams. The lanugo and vernix caseosa are formed. The skin is of a duskj^ cinnabar- 
red color. The meconium is darker. The scrotum is empty, small, and red ; the labia 
majora are prominent and held apart by the projecting clitoris. The pupillary mem- 
brane is present and readily recognized. The length of the humerus and radius is 3.5 
cm. ; of the ulna, femur, tibia, and fibula, each 3.7 cm. 

At the twenty -eighth iceek the embrj'-o is 36.4 to 39 cm. long and weighs 1,500 to 
1,750 grams. The hair is more abundant and longer. The great fontanelle measures 
about 4 cm. in its long diameter, and all of the fontanelles are readily perceived. The 
skin is of a dirty-reddish color and abundantly beset with the lanugo and vernix caseosa. 
The large intestine contains much meconium. The humerus is 4.5 to 5 cm. long; the 
radius 3.7 cm. ; the ulna 4 cm. ; the femur, tibia, and fibula, each 4.2 to 4.6 cm. 

At the thirty-second iceek the embryo is 39 to 41.5 cm. long and weighs 1,500 to 
2,500 grams. The skin is lighter in color; the pupillary membrane has disappeared. 
The testicles are in the scrotum or the inguinal canal ; the labia are still widely apart 
and the clitoris is prominent. The nails reach nearly to the ends of the fingers. The 
humerus is 5 to 5.2 cm. long; the radius 4 to 4.2 cm. ; the ulna 4.8 to 5 cm. ; the femur 
5.2 cm. ; the tibia and fibula, each 4.8 to 5 cm. The last sacral vertebra begins to 
ossify. 

At the thirty-sixth iceek the embryo is 44.2 to 46 cm. long and weighs about 3,000 
grams. The scrotum begins to become wrinkled and the labia commence to close. The 
hair becomes more abundant, while the lanugo begins to diminish in amount. 

At the fortieth week the foetus is fully developed and the term of its intra-uterine 
life accomplished. 

Size, Age, and Characters of the Xew-born Child. — The fresh corpse of anew- 
born child at term no longer resembles that of the immature foetus. The skin is firm 
and pale, like that of an adult. The lanugo has disappeared except on the shoulders. 
In the majority of cases the hair on the head is 1.5 to 2 cm. long. The great fontanelle 
is, in the average, 2 to 3 cm. long. As determined by ananalj^sis of 661 cases, the aver- 
age length is 50 cm. the weight 3,256 grams. The nails are hard and reach to the tips 
of the fingers, but not to those of the toes. The cartilages of the ears and nose are hard. 
The labia are more nearly closed. An ossification centre in the lower epiphysis of the 
femur should be sought for, as its presence is one of the most reliable signs of the ma- 
turity of the foetus. If it is absent, the foetus is, as a rule, not more than thirty-seven 
weeks old ; but in rare cases it may be absent at term. A centre of ossification 1 mm. 
in diameter indicates an age of 37 to 38 weeks, if the child was born dead or died soon 
after birth. Rarely it is no larger than this at term. A diameter, at birth, of 1.5 to 9 
mm. indicates an age of 40 weeks. A diameter of more than 9 mm. indicates, as a rule, 
that the child has lived some time after its birth; a less diameter than 7 mm., however, 
does not prove the contrary. 

Twenty-four hours after the Urth of the child the skin is firmer and paler. The um- 
bilical cord is somewhat shrivelled, although still soft and bluish in color. From the 
second to the third day the skin has a yellowish tinge and the cuticle sometimes appears 
cracked. The umbilical cord is brown and dry. From the third to the fourth day the 
skin is yellower, and the cuticle is apt to separate from the skin. The umbilical cord 
is of a brownish-red color, flattened, semi-transparent, and twisted. The skin around 
its insertion is red and congested. 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 41 

General Inspec:tion. — The head should be examined for the marks of injuries. 
Very commonly some portion of the scalp will be found swollen and iniiltrated with 
blood and serum. This may be the caput succedaneum formed during delivery. The 
mouth and nose should be examined for the presence of foreign bodies which might 
have caused suffocation. 

The neck should be examined for marks of strangulation. The umbilical cord may 
be twisted around the child's neck and strangle it. The mark left by the cord is usu- 
ally continuous, broad, not excoriated, sometimes accompanied by ecchymoses in the 
skin. 

The surface of the body should be examined for the presence of vernix caseosa, 
blood, marks of injury, and the existence of putrefaction. It should be remembered 
that putrefaction is apt to commence earlier in the bodies of young children than in 
those of adults. 

The umUUcal cord may be cut or torn. It usually separates by the fifth day, some- 
times not until the tenth. If the umbilicus is cicatrized and healed, the child has prob- 
ably lived for three weeks. A zone of redness around the insertion of the cord may ex- 
ist previous to birth. Redness and swelling (which may disappear after death) with 
suppuration can be found only in a child which has lived for several days. The drying 
and mummification of the cord may take place as well in dead as in living children. 
It is possible for a child to die by haemorrhage from a cut or torn cord, either before or 
after it has breathed. The umbilical vessels should be examined, as they may be the 
seat of umbilical infection. 

The extremiiies may exhibit fracture of the bones. These may occur during intra- 
uterine life, from injuries to the woman or from unknown causes; or may be produced 
by violence in delivery, or by injuries after birth. 

Internal Examination. — The Head. — The fontanelles and sutures should first be 
examined as to their size and for penetrating wounds. An incision should then be made 
through the scalp across the vertex, and the flaps turned backward and forward as in 
the adult. With a small knife the edges of the bones should be separated from the 
membranous sutures and the dura mater, beginning low down in the frontal and going 
back into the lambdoidal suture on either side. The bones are then drawn outward and 
cut through around the skull with strong scissors. The brain is removed and examined 
as in the adult. ^ 

Effusions of blood — cephalhaematoma — may be formed, soon after birth, between 
the pericranium and bone, or, more rarely, between the dura mater and bone. Clots are 
also found between the dura mater and skull ; between the dura and pia mater ; more 
rarely in the substance of the brain, as the result of protracted or instrumental deliveries, 
or of injuries after birth. 

The cranial bones may be malformed, or exhibit the lesions of rickets or caries, or 
be indented, fissured, or fractured. These latter lesions may be produced during intra- 
uterine life by injuries to the mother, by unknown agencies, by difficult deliveries, or 
by direct violence after birth. 

In cases of chronic internal hydrocephalus in young children, in which the ventri- 
cles are much dilated and the brain substance is thinned over the vertex, the brain is very 
apt to be torn in removal, and the amount of dilatation thus becomes difficult of deter- 
mination. It is, therefore, better in such cases to place a pail of water beneath the head, 
or even immerse the latter in it, and remove the brain in the water. In this way it floats 
after removal, supported on all sides. It may now be opened in the water and the ex- 
tent of the lesion determined at once, and parts saved for microscopical examination. 

If it be desired to preserve the brain for demonstration of the lesion or for a museum 
specimen, it should be transferred unopened to a large jar containing fi ve-per-cent. forma- 
lin. A portion of the ventricular fluid should now be removed with a syringe provided 
with a small canula, and replaced by formalin. This may be done by puncturing the 
ventricles from below. The fluid in the jar, as well as in the ventricles, should be 
changed in forty -eight hours. The brain may then be cut transversely across, when 

' Or an incision through the bones with a fine saw may be made as in the adult. 



42 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 

the degree of dilatation of the ventricles, etc., will be revealed. The weight of the 
brain, according to Bischoff, is 380 grams. 

It is normally much softer and pinker than in the adult, the pia more delicate ; both 
may be much congested or anaemic without known cause. The ventricles contain very 
little serum. Malformations, apoplexies, hydrocephalus, simple and tuberculous inflam- 
matory lesions, are to be looked for. 

The Spinal Cord. — Extravasations of blood between the membranes of the cord 
may occur from the same causes as those in the brain. Spina bifida is the most fre- 
quent malformation. 

The Thorax and Abdomen. — These are opened as in the adult. The peritoneal 
camty contains a very little clear serum. A red fluid may be produced by decomposi- 
tion. The peritoneum is often the seat of intra-uterine inflammation. 

The Biaphragni. — In still-born infants its convexity reaches to the fourth or fifth rib. 
After respiration it reaches a point between the fourth and seventh ribs. Its position 
is, however, so variable that it is of little diagnostic importance. 

The Thorax. — The thymus gland, at this period very large, occupies the upper por- 
tion of the anterior mediastinum, covering the trachea and large vessels. Its average 
weight is about 15.5 grams. It is usually about 5 cm. long, 3.8 cm. wide at its lower 
part, and about .63 to .85 cm. in thickness. It maybe hypertrophied and compress 
the large vessels, or be inflamed and suppurating. 

The heart lies more nearly in the median line than in the adult. It w^eighs from 
20 to 24 grams. The ventricular walls are of nearly equal thickness. The pericardium 
contains very little serum. A considerable quantity of red fluid may accumulate here 
as a result of decomposition. There may be small extravasations of blood beneath the 
pericardium in still-born children and in those born alive. Pericarditis with effusion of 
serum and fibrin, and endocarditis with consequent changes in the valves, may exist 
before birth. Malformations and malpositions of the heart and large vessels are not 
infrequent. The time of closure of the foramen ovale and the ductus arteriosus varies 
very widely in different cases. 

The pleural cavities contain very little serum, but decomposition may lead to the 
accumulation of a considerable quantity of red fluid. Small extravasations of blood 
in the subpleural tissue may be found in children who have died before birth and after 
protracted labors. Inflammation, with exudation of serum, fibrin, and pus, may exist 
before birth. 

The lungs in a still-born child are small, do not cover the heart, are situated in the 
upper and posterior portion of the thorax, are of a dark-red color and of firm, liver-like 
consistence, and do not crepitate. In a child born alive, and which has respired freely, 
the lungs fill the thoracic cavity, but do not cover the heart as much as in the adult ; 
they are of a light-red or pink color, and crepitate on pressure. If respiration has been 
incompletely performed, we find various intermediate conditions between the foetal and 
inflated states. 

If any doubt exists as to respiration having taken place, it is customary to employ 
the hydrostatic test. This is done by placing the lungs, first together, then separately, 
and afterward cut into small pieces, in water. It is commonly said that if they sink 
the child has not breathed ; if they float it has. This test is not, however, a certain 
one.^ 

The lesions of inflammation, and vesicular and subpleural emphysema, may be 
found in the lungs of new-born children. 

The pharynx should be opened and examined for foreign bodies. 

The larynx and trachea should be examined for the lesions of inflammation and for 
injuries to the cartilages. 

The thijroid gland weighs about 12 grams. It may be so enlarged as to interfere 
with respiration. 

The Abdomen. — The kidneys are lobulated and proportionately larger than in the 
adult. Thoma estimates the average weight of both organs together as 23.6 grams. 

^ See works on medical jurisprudence. 



THE METHOD OF MAKING POST-MORTEM EXAMINATIONS. 43 

There may be ecchymoses on their surface ; inflammation ; deposits of uric acid and 
urates in the tubules of the pyramids ; cystic dilation of the tubules, sometimes reach- 
ing an enormous size. There may be absence or retarded development of one kidney. 
Malformations and malpositions of the kidneys are of frequent occurrence. 

The adrenals are large. They may be dilated into large cysts filled with blood. 

The spleen is large and firm. Its average weight is about 11 grams. It may be 
abnormally enlarged, and its surface is sometimes covered with fresh inflammatory 
exudations. 

The Intestines. — In the small intestines, inflammation and swelling and pigmenta- 
tion of the solitary and agminated follicles (lymph nodules) are sometimes found. The 
large intestine usually contains meconium, but this may be evacuated before or during 
birth. The sigmoid flexure is not as marked as in the adult. 

The formation of gas in the stomach and intestines does not usually take place until 
respiration is established. If decomposition has commenced, however, gas may be 
formed as a part of the process. 

The liver is of a dark-red color, is large, and contains much blood. Its size dimin- 
ishes after respiration is established. Its average weight is 118 grams. The size is so 
variable, before and after respiration, that it gives little information as to the age of the 
child. Large extravasations of blood are sometimes found beneath the capsule of the 
liver without known cause. A variety of pathological conditions, fatt^y and waxy de- 
generation, gummy tumors, etc., may be found. 

The bladder may be full or empty, both in still-born children and in those which 
have breathed. Dilatation and hypertrophy may exist during intra-uterine life. 

Generative Organs. — The external generative organs in both males and females are 
more prominent than in adults. The ovaries are high up in the pelvis and large; the 
cervix uteri is long; the body small and lax, resting forward against the bladder. 
Phimosis in the males is the normal condition. Malpositions and retarded development 
of the testicles should be noticed. It should be observed whether the anus is perforate. 

The Bones, in suspected cases, should be examined for the lesions of inflammation, 
rickets, and S3"philis. 

Preservation. — The various foetal tissues may be preserved by the same methods 
as are employed for those of the adult ; but as they are very delicate i\\Qj shoiild be 
handled with great care and the preservative fluids changed with sufficient frequency. 



CHAPTER II. 

THE LESIONS IN CERTAIN FORMS OF DEATH FROM 
VIOLENCE: SUDDEN DEATH. 

The Lesions in Certain Forms of Death from Violence. 

SUFFOCATION— ASPHYXIA. 

By suffocation is meant that condition in which, without direct press- 
ure on the larynx or trachea, air is prevented from penetrating into the 
lungs. The interruption of the function of respiration which is thus 
brought about induces the condition known as asphyxia. In this way 
many deaths from drowning and strangulation take place. 

The ways in which the supply of air may be cut off from the lungs 
are various. The mouth and nose may be closed by the hand, by plas- 
ters and cloths, by wrapping up the head in cloths, by covering the face 
with earth, hay, grain, etc. Foreign bodies may be introduced into the 
mouth, pharynx, and larynx. Blood may pass into the trachea from an 
aneurism or from a wound. The glottis may be closed by inflammatory 
swelling. Vomited material may lodge in the larynx. 

On the other hand, injury or disease of the medulla oblongata, or 
paralysis or spasm of the muscles of respiration from drugs, tumors 
pressing upon the air passages, or diseases of the lungs themselves, may 
induce asphyxia. 

External Inspection. 

The body should be examined for marks of violence, the cavities of 
the mouth and nose for foreign substances. 

The face may be livid and swollen or present a natural appearance. 
The conjunctiva may be congested and ecchymotic. There maybe small 
ecchymoses on the face, neck, and chest. The mouth often contains 
frothy blood and mucus. The tongue may be protruded. 

Internal Examination. 

The Brain and its membranes may be congested, or anaemic and oede- 
matous, or unchanged. The Blood throughout the body is usually dark- 
colored and fluid. 

The Larynx may contain foreign bodies which have induced the suffo- 
cation. The mucous membrane of the larynx, trachea, and bronchi may 
be congested and sometimes ecchymotic : these passages contain frothy 
blood and mucus. The Lungs are usually congested and oedematous, but 
sometimes do not differ from their ordinary appearance. There may be 



THE LESIONS IN CERTAIN FORMS OF DEATH FROM VIOLENCE. 45 

small patches of emphysema near the surface of the lungs. Sometimes, 
especially in infants, small ecchymoses are found in the costal and pul- 
monary pleura. 

The Heart usually presents its right cavities full of blood, its left 
cavities empty ; but to this there are frequent exceptions. 

The Abdominal Viscera are usually congested. 

DEATH FROM STRANGULATION— HANGING. 

Strangulation is eifected by the weight of the body in hanging, by 
pressure on the neck with the hands or by some other object, or by con- 
striction of the neck with a cord or ligature of some kind. Death usually 
occurs by asphyxia, or by asphyxia combined with the effect of the cut- 
ting- off of the blood supply to the brain by pressure on the large vessels 
of the neck. In some cases of hanging, death ensues as a result of frac- 
ture or dislocation of the cervical vertebrae. 

External Inspection. 

The face may be livid and swollen, the eyes prominent, the lips 
swollen, and the tongue protruded. These appearances are, however, 
often absent. Erection of the penis, ejaculation of semen, and evacu- 
ation of faeces and urine are frequently observed. 

In many cases marks are left upon the neck by the objects which have 
directly produced the strangulation. In cases of hanging, the mark 
about the neck varies considerably in position, direction, and general 
characters, depending upon the kind of ligature employed, the time of 
suspension, period after death at which the observation is made, etc. 
The most common mark left by a cord about the neck is a dry, dense, 
brownish furrow, whose breadth corresponds but in a very general way 
with the diameter of the cord. In some cases, according to Tidy and 
others, there may be no mark at all if the hanging be quickly accom- 
plished with a soft ligature and the body cut down immediately after 
death. There may be abrasions and ecchymoses of the skin at the seat 
of ligature. 

In cases of strangulation by the fingers the mark on the neck may 
correspond in a general way to the shape of the fingers. 

The application of the same forces immediately after death may pro- 
duce the same marks as when death is induced by them. 

Internal Examination. 

The Brain and its membranes may be congested, or there may be ex- 
travasation of blood, or there may be no abnormal appearances. 

The Necli. — In some cases there is effusion of blood beneath the liga- 
ture, rupture of the cervical muscles, fracture of the os hyoides and car- 
tilages of the larynx, fracture and dislocation of the cervical vertebrae. 



46 THE LESIONS IN CEHTAIN FORMS OF DEATH FROM VIOLENCE. 

rupture of the internal vertebral ligaments and of the inner and middle 
coats of the carotid arteries. Similar changes may be produced in the 
dead body by the use of great violence. 

If death occur from asphyxia, the internal lesions are similar to those 
described above. In some cases — for example, where death has occurred 
from fright or shock — the results of post-mortem examination are en- 
tirely negative. 

DEATH FROM DROWNING. 

In examining the bodies of persons who have been drowned, it is 
necessary to bear in mind a number of questions which may arise: 
Whether the person came into the water alive or dead? How long a 
time has elapsed since death'? Whether the person committed suicide, 
or was drowned by accident, or was murdered? These questions are to 
be solved sometimes certainly, sometimes with probability, sometimes 
not at all, by the post-mortem examination. Persons dying in the water, 
to which condition the term drowning is commonly applied, may die 
from asphyxia, from exhaustion, from fright or syncope, from disease of 
the heart, apoplexy, injuries, etc. While in the majority of cases as- 
phyxia is a predominant or imx^ortant factor in death by drowning, the 
conditions under which death occurs are so apt to be complex that in the 
minority of cases only are the lesions of pure asphyxia found after 
death, while in most cases the bodies present the more or less well-marked 
lesions of asphyxia together with those indicative of complicating con- 
ditions. There are no post-mortem conditions which alone are abso- 
lutely characteristic of drowning, and it is only by considering all the facts 
elicited by the autopsy together that any just conclusion can be arrived 
at. It should always be borne in mind, moreover, that even the most 
characteristic of the evidences of drowning are apt to be modified or to 
disappear as decomposition goes on. 

External Inspection. 

Post-mortem rigidity usually sets in early, sometimes immediately 
after death. Decomposition progresses, especially in summer, with un- 
usual rapidity in bodies which have been removed from the water. Fre- 
quently, but by no means constantly, the peculiar roughening of the 
skin, known as goose skin (cutis anserina), is found, but this may occur 
after death from other causes. A light, lathery froth, either white or 
blood-stained, is frequently seen about the mouth and nostrils within 
twelve to twenty-four hours after removal of the body from the water, 
but it may be absent, and may be seen after death from other causes. 
After the body has lain for several hours in the water (twelve to twenty- 
four) the thick skin of the palms of the hands and soles of the feet may 
become macerated and thrown into coarse wrinkles, just as it may after 
prolonged soaking during life, or in a dead body thrown into the water. 
The penis and nipples may be retracted, and the scrotum shrunken, but 
this is not constant nor characteristic. 



THE LESIONS IN CERTAIN FORMS OF DEATH FROM VIOLENCE. 47 

If the person has struggled in the water and clutched at objects 
within his reach, there may be evidences of this in excoriation of the 
fingers or in the presence of sand, weeds, etc. , under the nails or grasped 
in the hands. 

External marks of injury, bruises, etc., should be sought for, since 
persons in dying, or on being thrown into the water with homicidal 
intent, may have died from the violence, and not, strictly speaking, from 
drowning. It should also be borne in mind in such complex cases that 
injuries, not in themselves fatal, may, when the body is in the water, 
prove so on account of the inability of the person to rescue himself or 
gain time for recovery from the injury, and that then the struggle for 
breath may be but slight, and the more prominent signs of drowning but 
little marked. 

Internal Examination. 

The Brain. — Congestion of the brain and its membranes is found only 
in a small proportion of cases. 

The Blood, when death occurs from asphyxia, is usually fluid through- 
out the body and of a dark color, as in asphyxia from other causes. 

The Air Passages. — In persons who die from asphyxia the mucous mem- 
brane of the larnyx, trachea, and bronchi is usually congested, and the 
air x>assages contain a variable quantity of bloody or mucous froth. In 
persons dying in the water from other causes than asphyxia, these ap- 
pearances are absent. Foreign substances from the water, such as sand, 
weeds, etc., or materials regurgitated from the stomach, may find their 
way into the air passages during the act of drowning or as a post-mortem 
occurrence. Thus, in bodies washed about the bottom, sand or mud may 
get into the air passages for a certain distance, from the mechanical ac- 
tion of the water. 

The Lungs in typical cases are distended so that they fill the thorax 
and cover the heart. The increased size is due partly to congestion, 
partl}^ to the presence of the fluid in which the person was drowned, 
which is often inspired during the act of drowning, a'^d i3artly to the 
distention of the air vesicles with air. In cases of drowning in which 
there is a struggle and water is breathed in, the lungs may contain con- 
siderable fluid ; but, as a result of decomposition, this may find its way 
in greater or less quantity into the pleural cavities by transudation, 
leaving the lungs comparatively empty. It should be remembered, how- 
ever, that a considerable quantity of reddish fluid may collect in the 
pleural cavities under other conditions than drowning, through a post- 
mortem change, by transudation from the blood-vessels and other ad- 
jacent tissue. 

The Heart. — In those who die from asphyxia the right cavities are 
usually filled with fluid blood, while the left cavities are emj)ty. But 
when death is due to complex causes this may not be the case. 

The Abdominal Viscera may be congested in persons who die from 
asphyxia. 



48 THE LESIONS IN CERTAIN FORMS OF DEATH FROM VIOLENCE. 

The Stomach. — The fluid in which the person was drowned, sometimes 
mixed with sand, weeds, etc., maybe swallowed during the act of drown- 
ing. Sand may wash for a short distance into the oesophagus after 
death, in bodies washing about the bottom. 

In persons dying in the water from syncope, shock, etc. , we may find 
no lesions. When the death is partly due to asphyxia and partly to other 
causes, the lesions may vary in numerous ways, which need not be de- 
scribed here. 

In important cases of doubtful drowning it is desirable carefully to 
collect and save some of the fluid from the lungs and stomach for micro - 
chemical examination, since the identification of these fluids with those 
in which the person was presumably drowned will often give certainty 
to an otherwise doubtful case. 

For the detailed consideration of the anatomical diagnosis of drown- 
ing, the changes which bodies dead from drowning undergo from decom- 
position, and the factors bearing on the question of suicide, homicide, 
etc., we refer to works on medical jurisprudence.' 

DEATH FROM ELECTRICITY. 

Lightning. — Persons who are struck by lightning may die instantly ; 
or may continue for several hours comatose or delirious, and then either 
die or recover ; or tl^ey may die after some time from the effects of the 
burns and injuries received. 

The post-mortem appearances are very variable. Sometimes there 
are no marks of external violence or internal lesions. Sometimes the 
clothes are burnt and torn, while the skin beneath them is unchanged. 
Usually there are marks of contusion and laceration, or ecchymoses, or 
lacerated, punctured wounds, or fractures of the bones, or superficial or 
deep burns. The track of the electric current may sometimes be marked 
by dark-red arborescent streaks on the skin. Fractures are rare. 

The internal viscera may be lacerated and disorganized from lightning. 

Artijieial Electrical Currents. — In death from powerful artificial elec- 
trical currents, either by accident, as in linemen and others, or in elec- 
trical executions, there may be local burnings of varying degree where 
the wires or electrodes come in contact with the skin. The clothes may 
be pierced with holes at the point of exit of the current. Internally 
there appear to be no marked or characteristic lesions, either gross or 
microscopical, in this form of death. Van Gieson and others have ob- 
served the occasional, but not constant, occurrence of small haemorrhages 
in the floor of the fourth ventricle, the significance of which is doubtful. 
Other petechial spots have been observed beneath the serous surfaces of 
the endocardium, pericardium, and pleura, and on the spleen. ' 

^ Tidy, "Legal Medicine," vol. ii. Guy and Ferrier, "Forensic Medicine." 
2 Van Gieson, " A Report of the Gross and Microscopical Examination of Six Cases 
of Death by Strong Electrical Currents." JN^ew York Medical Journal, May 7th and 
14th, 1892. Cunningham, "The Cause of Death from Industrial Electric Currents." 
New York Medical Journal, vol. Ixx., pp. 581 and 615, 



SUDDEN DEATH. 49 



DEATH FROM BUHNING. 



Death may be caused by the inspiration of smoke and flame ; by the 
drinking of hot fluids ; by the direct contact of flame or hot substances 
with the external surface of body. It may be due to the direct effect of 
the agents, to secondary afi'ections of the viscera, or to the exhaustion 
I)roduced by long-continued inflammation and suppuration. Sudden 
death may occur after extensive burnings of the skin.^ 

The burned skin divested of epidermis may present a peculiar red, 
hard, parchment-like appearance. If the patient have lived for some 
time, suppuration of the injured surface may ensue. Or there are small, 
bladder-like elevations of the epidermis. The base of these blisters is 
red, and they are surrounded by a red zone, or suppuration may have 
commenced. These appearances cannot be produced by heat applied to 
the skin after death. 

After death from severe burns there is apt to be congestion of the 
brain, and the thoracic and abdominal viscera. The lymph nodes and 
the lymphatic tissues throughout the body may be swollen and the seat 
of focal necrosis. There is usually albuminous degeneration of the liver 
and kidneys ; the spleen is swollen and the seat of focal necrosis. Focal 
necrosis in the bone marrow has been noted. There may be capillary 
thromboses, interstitial haemorrhages in the kidney, and leucocytosis. 
These lesions indicate the presence of toxic substances in the body fluids, 
and thus the general condition may be regarded as an instance of auto- 
intoxication. ^ 

Secondary lesion are not infrequent after severe burns. There may 
be oedema of the glottis, pseudo -membranous inflammation of the larynx 
and trachea, pneumonia, ulceration of the duodenum, and pyaemia with 
infarctions in the lungs, liver, s^jleen, and kidneys. 

Sudden Death. 

Some forms of sudden death from violence have been already consid- 
ered. Aside from these, by sudden death, in the ordinary sense, is usually 
meant ''the rapid and unforeseen termination of a latent acute or chronic 
disease." We shall not consider here sudden death either from violence 
or poisoning or in well-defined and evident acute or chronic diseases: it 
will be practicable only to enumerate some of the more common condi- 
tions under which sudden death may occur — and first in the adult. 

Circulatory Sijstem. — Heart — fatty degeneration, chronic myocardtiis, 
abscess of the myocardium, rupture, lesions of the coronary arteries, 
endocarditis, and pericarditis. Blood-vessels — arterio- sclerosis, aneu- 
rysms — especially intracranial, intrapericardial, abdominal, and pulmo- 

' For a studj" of Sudden death following severe burns, consult Silhermann, Vircli. 
Arch., Bd. cxix., p. 488, 1890. Bibliog. 

■^For a study of the visceral changes following extensive burns, consult Bardeen, 
Jour. Exp. Med., vol. ii., p. 501, 1897. Bibliog. 
4 



50 SUDDEN DEATH. 

nary ; congenital narrowness of the aorta, thrombosis and embolism of 
the pulmonary or cerebral arteries. 

Brain — meningitis, abcesses, and tumors. Very slight injuries of 
various parts of the body have been followed by sudden death, probably 
through inhibition. Syncope may terminate in death. 

Bespiratory System. — Foreign bodies lodging at the entrance to the 
larynx are not infrequently followed by immediate death without evi- 
dence of asphyxia. Hypertrophy of the thyroid, mediastinal tumors, 
pleurisy, and pneumothorax may lead to sudden death. 

Abdominal Viscera. — Eupture of visceral abscesses; perforation of ul- 
cers of the gastro -intestinal canal; rupture of the spleen, especially if 
the latter be enlarged as in malaria; extra-uterine gestation, retro- 
uterine hsematocele, and rupture of the uterus, are among the lesions 
not infrequently leading to sudden death. 

Sudden death is frequent in diabetes, in various forms of kidney le- 
sion and in alcoholism, and in association with the so-called lymphatic 
constitution. ' 

Sudden death in young children is most often associated with dis- 
orders of the respiratory system, thus differing from adults in whom le- 
sions of the circulatory system are of the greatest significance. Brouardel 
attributes sudden death in children usuallj^ to one of five principal causes 
— syncope, convulsions, asphyxia, pulmonary congestion, and intestinal 
disorders. A large thymus with the lymi^hatic constitution is frequent 
in cases of sudden death in young children.^ 

^ See reference, p. 337. 

2 For further details on this subject, consult Brouardel, ''Death and Sudden Death, " 
English translation, 1897 ; also works on forensic medicine. 



CHAPTER III. 

GENERAL METHODS OF PRESERVING PATHOLOGI- 
CAL SPECIMENS AND PREPARING THEM FOR 
STUDY. 

It is not our purpose in this section to give a complete account of the 
technical procedures required in the study of pathological specimens, 
since the methods are for the most part identical with those employed in 
the study of normal tissues, with which the student or practitioner is 
presumably already familiar. We wish simply to give a few brief hints 
as to the most useful methods for the ordinary purposes. Additional 
suggestions will be found in parts of the book dealing with special tissues 
and organs ; but for many methods which are invaluable for special pur- 
poses, and the technical details which are necessary for a skilful worker, 
one may consult Lee^s ^^Microtomists' Yade Mecum," fifth ed., 1900; or 
the ^^Pathological Technique'' of Mallory and Wright, 1897. 

The Study of Fresh Tissues. 

Although for the most part the conditions for the minute study of 
tissues are more favorable after these have been fixed and hardened by 
a suitable chemical agent, it is yet in many cases very important to ex- 
amine them in the fresh state. For this purpose they may be teased 
apart in a one-half -per-cent. solution of sodium chloride and mounted and 
studied in the same. Sodium chloride is also useful for the separation by 
dilution of the structual elements of fluids such as exudates, pus, etc. 

RAPID FIXATION AND FROZEN SECTIONS. 

A rapid fixation and development of detail in structural elements in 
fluids may be secured by allowing a drop of Carnoy's fluid or formalin 
to run under the cover glass and mingle with the salt solution, the flow 
being directed by a bit of filter iDaper put close to the edge of the cover 
glass on the side opposite to that on which the coloring fluid or fixative 
is added. 

Carney's Fluid. 

Saturated aqueous sol. methyl, green, 100 

Acetic acid, . .1 

Osmic acid, 0.1 

When an immediate diagnosis of a solid tissue is required, useful 
results may sometimes be obtained by a combination of the freezing 



52 PEESEEVING AND PEEPAEING PATHOLOGICAL SPECIMENS. 

method with the use of formalin as a fixative as suggested by Cullen. ' 
Any form of freezing microtome and either ether or liquid carbonic acid 
may be used. 

Cullen's procedure is as follows: The frozen sections are put in afive- 
per-cent watery solution of formalin for from three to five minutes; 
in fifty-per-cent alcohol for three minutes; in absolute alcohol for 
one minute. They are now washed in water, stained with hsematoxylin, 
decolorized in acid alcohol (one-per-cent hydrochloric acid), rinsed in 
water, contrast stained and dehydrated with eosin alcohol, cleared with 
creosote or oil of cloves, and mounted in balsam. The tissues shrivel 
considerably by this method. The disintegration of the sections after 
they thaw, and especially the considerable shrinkage which they undergo 
on treatment with alcohol, may both be largely obviated by spreading 
the sections, as they thaw, on an albumin fixative film upon a cover 
glass or slide — see below — and conducting the hardening and staining 
manii)ulations with the specimen in position upon the glass. 

HodenpyP has found that, when time permits, satisfactory results 
are secured by placing very small pieces of the fresh tissue for an 
hour in five-per-cent solution of formalin ; then, after washing out the 
formalin, making frozen sections in the usual way. The sections are 
now droi)ped for a moment into a solution of egg albumen of the follow- 
ing composition: 

Egg Albumen, 10 

Sodium Salicylate, . . . 1 

Water, . . . 30 

The sections are now spread on the slide, the excess of fluid being 
drained off, and are pressed against the glass with a bit of fine cheese 
cloth. They are finally fixed in place by a short immersion in strong 
alcohol. The section, now fast on the glass, is stained and mounted, in 
situ. This procedure, which can be carried out in a little more than an 
hour, gives a fair chance for an early morphological diagnosis in solid 
tissues, though the minute structural details are often much altered. 

Fixation : Hardening and Preservation. 

Alcohol is the most commonly employed fixative and hardening 

agent for routine purposes. It is used in the strength of from eighty to 

ninety-five per cent at first, the pieces of tissue to be hardened not being 

larger than 1 or 2 c. c. There should be in bulk many times as much 

alcohol as of tissue to be hardened. A little absorbent cotton may be 

placed in the bottle to keep the blocks of tissue from sticking to the 

bottom. After twenty-four hours the alcohol should be renewed. On 

the third day the tissue is transferred to ninety-seven-per-cent or to 

absolute alcohol for comj)letion of the hardening, which will usually be 

within five or six days. 

^ Cullen, Johns Hopkins Hospital Bulletin, April, 1895. 

" Hodenpyl, "A Modification of Cullen's Method of Preparing Fresh Sections for 
Microscopic Work," Medical Record, March 5, 1898. 



PRESERVING AND PEEPAKING PATHOLOGICAL SPECIMENS. 53 

While for many purposes other and more delicate methods of harden- 
ing tissues are to be recommended, alcohol is most useful for most solid 
tissues in which bacteria are to be sought: for such specimens as are not 
quite fresh and in which the process of decay is to be immediately 
checked, and in general for tissues in which the determination of topo- 
graphical features for diagnostic or other purposes is the chief end in 
view. 

Formalin, or formol, is the trade name for a forty-per-cent aqueous 
solution of formaldehyde. In diluted solutions it is a valuable fixative 
for delicate tissues. It is most commonly used in a solution of 5 parts 
(of the commercial formalin) to 100 of water. The fresh tissues, in 
small pieces, are put in this solution for forty -eight hours, the fluid 
being renewed at the end of twenty-four hours. They are then trans- 
ferred to sixty-per-cent alcohol for twenty-four hours, and the harden- 
ing is completed with strong alcohol. 

MtJLLER's Fluid which has been much used as a hardening agent 
has the following composition : 

Potassium Bichromate, .2 parts 

" Sulphate, 1 part 

Water, . . .100 parts 

Miiller's fluid is now most often used in combination with other 
fixatives. 

Thus OrWs Fluid, which is Miiller's fluid to 100 parts of which 10 
parts of commerical formalin are added, is a most valuable agent for 
fixing and hardening delicate cells. The mixture should be made at the 
time of using because it soon changes. The pieces of tissue should be 
small, the fluid largely exceeding the tissue in bulk. The hardening is 
completed in three or four days, when the specimens should be thor- 
oughly washed and preserved in eighty-per-cent alcohol. 

OsMic Acid is of great value, especially in combination, for the 
hardening of small portions of delicate tissues, since it serves to flx the 
elements in a nearly normal condition and stains them brown or black. 
Osmic acid stains fat black and on this account is a valuable agent for 
the detection of this substance in the tissues. It is generally used in 
one-per-cent aqueous solution, the tissues, in very small pieces and when 
quite fresh, being placed in it and allowed to remain for twenty-four 
hours. They are now washed thoroughly in water and may be preserved 
in eighty-per-cent alcohol. 

Flemming^s Osmic Acid Mixture. — For the purpose of flxing delicate 
tissue elements to show minute structural detail, such as mitotic figures, 
this mixture is of great value. It is made of 

One-per-cent solution of Chromic Acid, 15 parts 

Two-per-cent solution of Osmic Acid, 4 " 

Glacial Acetic Acid, .1 part 

This mixture does not keep well, and hence should be made up in small 
quantities. Small portions of tissue should soak in the mixture for 



54 PRESERVING AND PREPARING PATHOLOGICAL SPECIMENS. 

twenty-four hours, then, after thorough washing in water, they are put 
for twenty-four hours in seventy -per -cent alcohol, and then transferred 
to strong alcohol, in which they are kept. 

Corrosive Sublimate. — This is a most excellent fixative for delicate 
structures. 

A convenient preparation is Lang^s Solution. Its formula is : 

Mercuric Chloride, 5 gms. 

Sodium " . ■ 6 " 

Hydric Acetate, Glacial, 5 c.c. 

Water, . . . . . . . . . .100 c.c. 

The tissues should remain in sublimate solution, as a rule, not longer 
than from one to three hours. 

Specimens fixed in sublimate develoj) a mercurial precipitate, do not 
stain well, and become brittle unless the excess of sublimate is removed. 
This can be largely done by prolonged washing in running water. But 
it is much more easily and certainly accomplished by the chemical action 
of dilute iodine solution. The specimen is removed from the sublimate 
mixture and put at once into seventy -per -cent alcohol. To this is added 
from time to time a sufficient quantity of saturated alcoholic solution of 
iodine (or tincture of iodine) to give the alcohol a moderately deep 
iodine color. At first this color gradually disappears, and the iodine 
solution should be repeatedly added until the color persists. The speci- 
mens are now transferred to seventy-per-cent alcohol, and after twenty- 
four hours, to strong alcohol. 

Zenker^ s Fluid is a good fixative and acts rapidly. It is a combina- 
tion of Miiller's fluid and corrosive sublimate with acetic acid. Its 
formula is : 



Potassium Bichromate, 
Sodium Sulphate, 
Mercuric Chloride, . 
Hydric Acetate, Glacial, 
Water, 



2 parts 
1 " 
5 " 
5 " 
90 " 



The acetic acid should be added at the time of using, since the com- 
plete mixture readily decomposes. Small pieces of tissue may be har- 
dened in this solution in from twenty -four to forty -eight hours. They 
should then be carefully washed and preserved in eighty -per-cent alcohol. 
The use of iodine to remove the excess of sublimate, as described under 
Lang's solution above, is desirable here also. 

Pathological specimens which occur, or are isolated in the form of 
membranes, should be stretched with pins on a piece of wood or flat 
cork before being immersed in the preservative fluids. Minute struc- 
tures, such as occur in exudates from the mucous membranes and in 
cyst fluids, renal casts, etc., may be hardened in Flemming's osmic acid 
mixture or in formalin followed by alcohol. Under these conditions re- 
newals or changes of the fluids may be effected in tubes by the use of the 
centrifugal machine. The specimens may finally be preserved in eighty- 
per-cent alcohol. 



PRESERVING AND PREPARING PATHOLOGICAL SPECIMENS. 55 

Decalcifying. 

Bones which are the seat of lesions, and calcified tissues, must be 
freed from lime salts before thin sections can be made. 

Tissues which are to be decalcified should be in small pieces and first 
well hardened in alcohol or in Orth's fluid. 

Eapid decalcification may be secured by the combination with nitric 
acid of phloroglucin, the latter agent preventing the swelling of the tissue 
elements. One gram of phloroglucin is dissolved with gentle heat in 5 
c.c. of nitric acid. This solution, when effervescence has ceased, is of a 
ruby-red color. To this are added 70 c.c. of strong alcohol and 30 c.c. 
of water. This solution deteriorates with age. Small pieces of bone or 
other tissue are suspended by thread in relatively large quantities — at 
least twenty times the bulk of the specimens — of this fluid. In from one 
to twenty-four hours, depending upon the size of the piece of bone, 
the decalcification is usually complete. The specimen is now washed 
thoroughly in running water ; put for twenty-four hours in eighty-per- 
cent alcohol and then in strong alcohol. Bone decalcified in this way 
may be stained with hsematoxylin and eosin. 

Embedding and Section Cutting. 

EMBEDDING. 

Some dense tissues, after being well hardened, are sufficiently solid to 
permit of thin sections being made from them without further prepara- 
tion, but in most cases very thin sections cannot be prepared without fill- 
ing the interstices of the tissue with some embedding material, which 
gives it greater consistence and holds the tissue elements firmly in their 
natural relations to one another, while the section is being made. Cel- 
loidin and paraffin are the most generally useful materials for this 
purpose. 

Celloidin, a non-explosive, purified form of gun-cotton, is best ob- 
tained in the form of thin shavings, since in this form it is most easily 
dissolved. A six-per-cent solution is made in equal part of sulphuric 
ether and strong alcohol. The specimen in small pieces is soaked for 
twelve hours in this celloidin solution, diluted with an equal amount of 
the mixture of alcohol and ether, then for twelve hours in the six-per- 
cent celloidin solution. If the specimen be small and require but little 
support, it may now be laid directly on the end of a small block of wood 
or cube of glass or vulcanite, and a few drops of celloidin poured around 
it. In most cases, however, it is better to make a small paper box, in 
which the specimen is placed in a proper position, and the celloidin 
poured in around it so as completely to enclose it. In either case a con- 
siderable quantity of celloidin should be poured around the specimen, 
since the celloidin shrinks considerably in hardening. The paper box 
may be made by winding a strip of thin paper around the end of the 



56 PRESERVING AND PREPARING PATHOLOGICAL SPECIMENS. 

siipportiug block, allowing it to project for a sufficient distance beyond 
the end. The pajDer is held in place by a rubber band. We have thus 
a cylindrical box with a solid bottom projecting below it by which the 
whole can be held in the clamp of the microtome. 

After the specimen, either free on the end of the block or in its box, 
is surrounded by celloidin, it should be allowed to stand for a short time 
exposed to the air, so that the celloidin may harden on the outside by the 
evaporation of the ether. If the temperature be high, the too rapid 
evaporation of the ether will cause bubbles to appear in the mass. This 
should be avoided by covering the specimen with a bell -jar. After the 
celloidin mass has acquired sufficient hardness on the outside to keep its 
shape, the whole should be placed in eighty-per-cent alcohol, in which 
the celloidin will harden and acquire a sufficient consistence for cutting 
in a few hours. When this is accomplished the paper may be stripped 
off, and the specimen is ready for sectioning. 

After the sections have been cut they may be stained in the usual way 
(see below) and mounted in glycerin or balsam. If mounted in balsam, 
the oil of origanum cretici is used for clearing. 

The uncut portion of tissue may be preserved, embedded in celloidin, 
by keeping it in eighty -i)er- cent alcohol. It is better, in permanent 
preservation of uncut celloidin-embedded specimens in bulk, to cut them 
off from the wooden blocks, since alcohol extracts from these a dark 
resinous material which colors the specimen and interferes with the 
staining of sections. If glass or vulcanite blocks be used, the whole may 
be kept in alcohol. 

Steimnow has recently devised a more rapid procedure in celloidin 
embedding. The celloidin solution is made by the following formula, a 
few day being required for dissolving : 

Celloidin, 15 gm. 

Oil of Cloves, . . 50 c.c. 

Ether, 200 " 

Absolute Alcohol, ......... 10 " 

The hardened specimen is transferred from strong alcohol to a small 
portion of the solution in a closed bottle. In from three to six hours a 
small piece of ordinary tissue is usually impregnated. It is then put in 
position on the mounting block and placed in pure chloroform. In this 
the projjer consistency for section cutting is secured in from two to three 
hours, after which the whole is transferred to eighty-per-cent alcohol, in 
which it may be kept. 

For further details and modifications of this method, see the original 
description. ' 

Paraffin. — For some purpose, especially when extremely thin 
though not large sections are required, paraffin embedding is almost in- 
dispensable. The sections of tissues thus embedded may be cut exceed- 
ingly thin (2 to 3 //, or even 1 ,a with the Minot-Blake microtome) and 

"^ Stepanow, Zeitsclir. f. wissenschaftl. Mikroscopie, Bd. xvii., p. 185, 1900. 



PRESERVING AND PREPARING PATHOLOGICAL SPECIMENS. 57 

when these are fixed to the slide and appropriately stained, the con- 
ditions for the study of cytological details are more favorable than by 
any other method. For the paraf&n technique the specimen should be 
small, say 1 c.c. as a maximum limit. The specimen, freed from the 
preservative fluid, is dehydrated by graded alcohols as follows: thirty 
per cent, fifty per cent, and seventy per cent, and finally ninety-five per 
cent, remaining in each of these alcohols for two or several hours, and is 
then placed in absolute alcohol. Complete dehydration of the specimen 
is indispensable for the success of this method, for if the slightest trace 
of water be left in the specimen, shrinkage or other artificial changes in 
the tissues are apt to occur, when the specimen is transferred to the clear- 
ing media preparatory to immersion in the melted paraffin. 

When the specimen is thoroughly dehydrated by absolute alcohol, it 
may be transferred to oil of cedar, remaining in this until it sinks and 
becomes clear. It is then immersed in a small dish or glass box of 
melted paraffin, kept in a constant temperature bath held at 52° C, 
where it remains until completely permeated by the paraffin. It is best 
to use paraffin which has a melting-point of 50° C. After the specimen 
has remained for a while in the first dish of melted paraffin, it is trans- 
ferred to a second dish of the same, in order to remove any clearing oil 
remaining in the specimen. The length of time of the paraffin immer- 
sion depends upon the size and density of the specimen ; as a general rule 
one-half hour is sufficient for small, soft, or porous fragments; an hour 
or one and a half hours for larger and denser tissues. A longer period 
of immersion may interfere with the finer structural details of the 
tissues. 

A small paper box considerably larger than the specimen itself is 
filled with melted paraffin, and with a warm needle or forceps the speci- 
men is transferred to the pai)er box and set in its proper position in the 
bottom, so that the surface to be cut lies against the bottom of the box. 
In order to avoid the slow cooling of the paraffin around the specimen in 
successive layers, which prevents the formation of a homogeneous mass, 
the paper box with its contents is quickly cooled by being put into cold 
water, even iced water. When the paraffin block is hard, it is fastened 
with paraffin on to one of the various discs belonging to the paraffin 
microtome, trimmed so as to have a rectangular cutting surface, and 
sections are cut with a dry knife. In order to stain these sections, 
the paraffin must be removed from the interstices ; this may be done with 
xylol. But when the supporting paraffin is removed from the sections 
they are liable to fall to pieces during the further staining and other 
manipulations. The only practical plan therefore with the great major- 
ity of paraffin sections is to affix them to a slide and carry them in this 
way through the various staining and mounting procedures. 

The best way of affixing delicate paraffin sections to a slide is by 
means of a thin film of albumen. Equal parts of white of egg and gly- 
cerin are thoroughly stirred together, filtered through paper, and a 
small amount of carbolic acid is added to prevent the growth of micro- 



58 PRESERYINGr AND PREPARING PATHOLOGICAL SPECIMENS. 

organisms. A very small drop of this albumen mixture is placed on one 
end of the slide, and with the ball of the finger or a fold of cloth, it is 
spread over the rest of the slide in as thin a film as possible. ^\Tiile this 
scarcely perceptible film of albumen fixative is still moist, the paraffin 
sections or the ribbons of serial sections divided into proper lengths, are 
laid upon the film and gently tapped down flat with a small camel 's-hair 
brush or the finger-tip. ' 

The slide with the attached paraffin sections is now heated over a 
flame, warmed just sufficiently to begin to melt the paraffin; this is a very 
delicate point in the operation. Just enough heat must be used to melt 
the paraffin and no more. If the slide be heated beyond this point, the 
sections may be shrunken or completely ruined. While the slide is still 
warm, it is plunged into a jar of xylol, oscillated to and fro a few sec- 
onds, then placed in a jar of absolute alcohol, then passed through a 
series of jars containing different strengths of alcohol — ninety -five per 
cent, seventy per cent, fifty per cent, and thirty per cent, remaining a 
few minute in each, and finally into water. Now the sections upon the 
slide may be stained in whatever way desired, carried up through the 
graded alcohols to absolute alcohol, then cleared in xylol or other clear- 
ing media, and mounted in balsam. 

Tightly covered cylindrical jars or wide-mouthed bottles are used for 
the better manipulation of paraffin sections, the whole slide being 
dropped into a bottle for staining as well as for the dehydration and 
clearing. 

SECTION CUTTING. 

This may be done in an emergency by the free hand with a razor 
ground flat on the lower side, but better sections can be obtained by 
means of a microtome, and practically all section cutting for microscop- 
ical purposes is done by some form of this instrument. One of the 
most useful of these is Thoma's. The Schanze microtome is also well 
adapted for general work, as are some of the American instruments 
made on the same plan. For cutting sections of tissues embedded in 
paraffin, and especially for serial sections, the Minot microtome of the 
improved form — the Blake-Minot microtome can, in skilled hands, cut 
sections 1 m in thickness — is excellent. 

^ Not infrequently very thin paraffin sections curl or become corrugated as they 
leave the knife, so that it is difhcult to place them fiat upon the fixative film. Should 
this occur, a few drops of water may be spread out in a thin layer over the albumen 
film while it is still moist on the slide, and the whole slide, with the layer of water upon 
its surface, is very gently heated over the flame — just sufficiently to soften but not to 
melt the paraffin. If the sections are then floated on the warm layer of water, they will 
uncurl and flatten out. The water is then drained off, when the flattened sections will 
lie flat upon the fixative film and remain fastened there. All traces of the water are 
now allowed to evaporate in the air ; or, the evaporation of the water may be hastened 
by exposure to a temperature four or five degrees below the melting-point of the 
paraffin. 



PRESERVING AND PREPARING PATHOLOGICAL SPECIMENS. 59 



Methods of Staining. 

Sections of hardened tissues may be stained for microscopical study 
in a variety of ways, but for routine work the double staining with 
hsematoxylin and eosin is most generally useful, and is applicable to 
nearly all cases. 

HEMATOXYLIN solutiou (Dclafield's) is prepared as follows: To 100 
c.c. of saturated solution of ammonia alum add 1 gram of hsematoxjdin 
crystals dissolved in 6 c.c. of ninety-five-per-cent alcohol. This solution 
is exposed to the light for a week, the color meanwhile changing from a 
dirty red to a deep bluish-purple color. ' Then 25 c. c. each of glycerin 
and wood naphtha are added. This mixture is allowed to stand for a day 
or two and is then filtered, and the filtration is repeated at intervals until 
a sediment no longer forms. 

The solution is now ready for staining, the best results being obtained 
by diluting the fluid with from ten to twenty times its bulk of water. 
The sections are immersed in the fluid, and allowed to remain until they 
have acquired a distinct purple color which persists after rinsing in 
water. They are now placed for a moment in a dilute alcoholic solution 
of eosin, and then mounted in glycerin which has been colored lightly 
with an alcoholic solution of eosin. In this way the nuclei of the cells 
will be stained of a purple color, while the cell bodies, and to a certain 
extent the intercellular substance, will be colored a light rose-red. 

If specimens are to be mounted in Canada balsam, they are stained 
with hsematoxylin as before, and the eosin staining is done by tinging, 
with a saturated alcoholic solution of eosin, the alcohol with which the 
final dehydration of the si^ecimen is accomplished. A similar result 
may be obtained by tinging the oil of cloves or origanum with which the 
clearing of the sections is effected. 

Iron Hcematoxylin (Ifeidenhain^ s) . — Sections are soaked for an hour 
in a two-per-cent solution of ammonia sulphate of iron, then rinsed with 
water and put for an hour in a one-half-]3er-cent aqueous solution of 
hsematoxylin (prepared by heating) ; again rinsed and put again in the 
iron solution, in which the color gradually fades. The section must be 
watched during the process of the differentiation which takes place in 
the iron solution, and when this is accomplished to a proper extent the 
section is thoroughly washed in running water and mounted in the usual 
waj^ This method is especially valuable for the study of nuclear struc- 
tures, the color of these ranging from blue to black, depending upon the 
length of time of immersion in the stain and the grade of differentiation. 

By the use of this method, micro-organisms may be stained black, and 
in this condition are, as Learning has shown, well fitted for the purposes 
of photomicrography. 

^ The time required for this " ripening " of the solution may be spared by the use of 
hsematin in the place of haematoxylin. 



60 PRESERVINa AN^D PREPARING PATHOLOGICAL SPECIMENS. 

PiCRO-AciD FucHSiN (Van Gieson^s Stain). — This double stain, first 
suggested by Yan Gieson, especially for the nerve tissue, has wide ap- 
plications in both normal and pathological histology, and is most useful 
when following a deep hsematoxylin stain. 

It colors the fibrillated connective -tissue fibres and the neuroglia in 
general a bright or garnet red, and also the axis cylinders and ganglion 
cells. Myelin, muscle fibres, and certain other cells are stained yellow, 
while the nuclei after the hsematoxylin stain are brownish-red in color. 
Van Gieson 's stain is also of value, although its limitations in this par- 
ticular are not yet fully determined, as a coloring-agent for hyalin, 
amyloid, colloid, and mucin in the tisues. As a differential stain for 
fibrillated connective -tissue fibres it is of value in the study of various 
tumors and especially of the sarcomata. 

It is commonly prepared in two strengths, the stronger for use espe- 
cially in nerve-tissue staining, the weaker for general purposes. The 
f ormulsB and method of using as suggested by Freeborn' are as follows : 

Picro-acid FucJmn, 
Stronger solution — 

One-per-cent aqueous solution Acid Fuclisin, . . . . 15 c.c. 
Saturated aqueous solution Picric Acid and Water, . each 50 " 

Weaker solution — 

One-per-cent aqueous Acid Fuchsin, 5 " 

Saturated aqueous solution Picric Acid, 100 " 

The tissues may be hardened either in alcohol, or in Orth's fluid, or 
in formalin. 

Sections are first stained deeply with hsematoxylin, washed in water, 
and put into the staining fluid, in which they remain for varying periods, 
depending upon the tissue and the strength of the stain, but in general 
from one to five minutes. The sections are now rapidly dehydrated by 
alcohol, cleared with oil of origanum, and mounted in balsam. 

Methylene Blue is a useful stain for many pur^Doses. The tissues 
may be hardened in Zenker's or Orth's fluid. Unna's polychrome meth- 
ylene blue is made by adding one part each of methylene blue and po- 
tassium carbonate to one hundred parts of water. This should stand 
for several weeks before use. The section is overstained and then de- 
colorized as follows : Stain for fifteen minutes or longer ; rinse in water, 
decolorize in one-half -per-cent acetic acid or in alcohol ; clear in xylol. 
Thionin or toluidin blue gives similar results. By the use of these stains 
the bodies of plasma cells (see p. 103) are colored bluish -violet, the nuclei 
blue. The granules of ^^mast cells'^ are stained red if the tissue be 
hardened in alcohol or Zenker's fluid, bluish if hardened in Orth's fluid. 

^Freeborn, Transactions New York Path. Soc, 1893, p. 73. 



PEESEEYING AND PREPARING PATHOLOGICAL SPECIMENS. 



Methods of Preserving Specimens for Gross Demonstration 

and for Museums. 

AYheu specimens of abnormal tissues or organs are to be preserved 
entire for exhibition in jars in a museum, the superfluous parts are first 
removed and the requisite dissections made. Then they are carefully 
placed in the i)osition and form which it is wished to preserve, by 
stuffing with horsehair or absorbent cotton and by the use of thread. 
WTien thus carefully adjusted they are either suspended or laid on a wad 
of absorbent cotton in sixty to eighty-per-cent alcohol, or in five-per- 
cent formalin solution. In this they usually become hard, and finallj^, 
after the removal of the temporary stuffing and braces, are trans- 
ferred for permanent exhibition to fresh, clear eighty-percent alcohol, 
or in case of formalin hardening to a fresh solution of the formalin, to 
which, if the jar is likely to be exposed to cold, a little glycerin is added 
to prevent freezing. This description applies especially to such speci- 
ments as have cavities to distend or display. 

The more simple specimens, such as the solid viscera, tumors, etc. , 
may be washed and hardened in sixty -per -cent alcohol or in formalin 
solution. 

In many cases an excellent hardening is obtained by injecting the 
preservative fluid through the blood-vessels. The lungs are well 
hardened by pouring the fluid through the trachea into the air spaces. 

Firm-walled cysts of various kinds are well iDreserved in a condition 
of distention by drawing off the natural contents through a fine canula 
and refilling with, and immersing in, formalin solution. Delicate cysts, 
such as echinococcus cysts, small embryos in their membranes, cystic 
kidneys, etc., may be preserved in a nearly natural condition in 
formalin. 

The Importance of Careful Fixation and Preservation. 

We would most urgently commend to the reader the importance of 
putting pathological specimens which are to be hardened and subse- 
quently examined microscopically, at the earliest possible moment into 
the preservative fluids, ichich should always be abundant. Furthermore, 
when specimens are large it is very desirable to cut them oi^en, so that 
the fluids may come into direct contact with the tissues. It should be 
borne in mind that immediately after death or the removal of parts from 
the body, especially in warm weather, changes commence in the tissues 
and progress very rapidly, so that in some cases a few hours' or even a 
few moments' delay will not only render subsequent microscopial ex- 
aminations difficult and unsatisfactory, but may lead to serious errors. 
Alcohol, and five-per-cent formalin are the most generally useful agents. 
Carbolic acid and glycerin should not be used, even for the temporary 
preservation of fresh tissue. They not only do not harden and preserve 



62 PEESEEVINa AND PREPARING PATHOLOGICAL SPECIMENS. 

the tissue elements, but they — especially glycerin — render them almost 
useless for microscopic examination. 

The not uncommon practice of wrapping a specimen in a cloth soaked 
in alcohol or carbolic acid, and permitting it to remain in this for hours 
or days, is of no use whatever in preserving specimens of which micro- 
scopic examinations are to be made. Almost equally useless is the too 
common practice of placing a specimen in a bottle which it nearly fills, 
and pouring a little x)reservative fluid around it. ]N'ot only should the 
proper fluids be used, but these should be abundant, and the specimen so 
prepared and arranged that they may come into direct contact with it. 



PART II. 

GENEEAL PATHOLOGY. 



INTRODUCTION. 

The successful pursuit of pathology — the scieuce which treats of 
disease— depends largely upon the clearness and accuracy of the stu- 
dent's knowledge of normal anatomy and normal physiology. 

Leaving aside as not indispensable, and at present not attainable, an 
accurate definition of life, it is important constantly to realize that the 
normal living body is a complex and delicate mechanism incapable of 
creating new forces but able, by means of its cellular and molecular or- 
ganization, to accumulate or store energy derived from without, releas- 
ing this under fixed and definite conditions. This storing of energy is 
possible by means of the capacity of living body-cells to build up com 
plex molecular combinations. These, owing to their instability, may be 
readily resolved into less complex and more stable combinations with 
the release of the stored-up energy. This it is which makes possible all 
expression of life. 

Many of the earlier views concerning life and death and health and 
disease, which have long since given way to more accurate concei)tions, 
still hold a certain sway among the thoughtless, perpetuated by tradi- 
tional forms of speech. One of these is that disease is an entity, some- 
thing foreign to the body which may enter from without, and with which 
the body may struggle and fight, which it may conquer or to whose rav- 
ages it may succumb. It will be wise for the student constantly to re- 
member that disease is not a thing, but a process. It is an abnormal 
performance of certain of the functions of the body. This may or may 
not be associated with appreciable morphological alterations of the body 
structure. It is those agencies and conditions to which the body has 
not adapted itself, which, swaying its normal capacities now one way and 
now another, induce the functional aberrations and structural alterations 
by which disease is manifested. 

It follows from this that the functional abnormalities and the struc- 
tural alterations which make up the signs, symi^toms, and lesions of dis- 
ease involve the expression of no new functional capacities which the 
normal body does not possess. These may be diminished or exalted, 
they may be perverted or abolished ; or the cells may now and then re- 
vert to forms and to phases of activity which the body has long since 
outgrown or largely suppressed in its slow adaptation to conditions of 
life which now constitute the normal. But the body in disease manifests 
no new functions, develops no new forms of energy, reveals no new ca- 
pacities. 

Thus, if pathology is to be for the student or the practitioner any- 
thing but a mass of more or less useful facts, he must learn to correlate 
5 



66 INTRODUCTION. 

its data with the facts and laws of normal morphology and normal phys- 
iology. While he should be conscious always on the one hand of the 
invisible molecular changes which underlie the manifestations of energy, 
and on the other will not ignore the details of gross morphology, his at- 
tention will be most constantly drawn to the cells as the life units upon 
which ultimately both the form and function of living things depend. 
He will realize that as the cells of the normal body are what they are in 
form and in function because of the conditions under which they have 
been slowly evolved, and are at the moment placed ; so when the condi- 
tions change and become abnormal, it is to the cells that he must look 
for an understanding of the aberrations and disturbances by which we 
recognize disease. 

In normal physiology attention is most keenly centred to-day upon 
the structure and performances of cells as the field richest in the prom- 
ise of significant revelations. So, also, in j)athology by similar methods 
and with equal persistence must the structure and performances of cells 
under abnormal conditions be studied if we are to hope with reason for 
a clearer comprehension of disease. This has long been recognized, and 
to the conception of the pathological processes as essentially cellular 
processes are due the great advances which this phase of biological science 
has made during the past few decades. But the newer knowledge of the 
cell, not as a membranous bag nor as a mere lump of protoplasm but as 
a complex machine whose various structural features are of the utmost 
significance, has greatly widened the fi,eld of cellular pathology. 

Manifestations of heredity which are displayed in the body as a 
whole have long been known. To-day we may and must take account 
of the marks of heredity in individual cell life. Not a few of what we 
call the aberrances of cells in disease are but the expression of cell traits 
and capacities latent in the environment which has become the usual and 
therefore the normal, but finding exi3ression as the sway of the body- 
organism is released under disturbances of its equilibrium. Thus cells 
thrown out of function may in a measure revert in character to less dif- 
ferentiated types, and cells long comparatively quiescent may under 
varying stimuli assume capacities and forms which they seemed to have 
outgrown. 

Of course in the pursuit of pathological morphology it is the dead 
body and dead tissues with which we are most often engaged. But these 
are of special interest only as they reveal structures or indicate processes 
which were maintained during life. So that he who can most closely 
correlate the knowledge of the living cells with his observations upon 
those which are dead will gain most from his morx3hological studies. 

^^ile the pathology of to-day is essentially a cellular pathology, 
while it is illuminating and convenient to consider the cells as physio- 
logical and structural units, maintaining a certain independence of ex- 
istence and function, it is nevertheless true that beyond their mere jux- 
taposition in the body, beyond a close mutual dependence upon the 
common blood supply and nerve control, there is a subtle and as yet 



INTRODUCTION. 67 

little understood transmission of physiological impulses from cell to cell. 
Whether this is by protoplasmic continuity or in some other way, we do 
not know. But it should not be left out of the account in some of the 
more complex and subtle problems which, in health as in disease, the 
life of the cell and the life of the body present. 

\\Tien we study the so-called causes of disease, we should remember 
always that underlying the manifestations of disease, as well as sustain- 
ing the correlated processes which we name health, are the complex and 
ceaseless chemical transformations which in both health and disease 
alike sui)ply the energy which sustains all exiDression of life. So that 
what we are wont to call the causes, whether external or internal, of dis- 
ease are really not primary causes, but liberating impulses or excitants 
which sway and modify the orderly transformations of energy constitut- 
ing health with those manifestations of perturbed function or altered 
structure, or both, on which our conceptions of disease are framed. 

Pathology, then, deals with the disturbances of function and the al- 
terations in structure in living beings, induced by unusual agencies and 
conditions. The functional disturbances thus induced are embraced as 
sym^Dtoms of disease in pathological physiology, which so largely dominates 
the scientific activities of the i^hysician, and forms the basis for the prac- 
tice of his art. The phenomena of i^athological physiology are in no 
sense opposed to those of normal physiology, but are their inevitable 
correlatives when the living body is placed under sufficiently abnormal 
conditions. FathoJogical morphology is concerned with the structural al- 
terations of the organism which may result from abnormal conditions. 
Pathological morphology deals with both the gross and the microscopic 
alterations of structure, and hence embraces both pathological anatomy 
and pathological histology. 

But alterations in structure are so closely associated with disturbances 
in function, and both are so constantly dependent upon the inciting fac- 
tors in disease, that an intelligent study of morphology necessitates a 
constant consideration of etiology and of certain phases of pathological 
physiology. 

It is customary and convenient in the study of pathology to consider 
together the general or elementary abnormal processes and conditions 
and the etiological factors in disease without reference to their special 
manifestations in particular organs or parts of the body. This division 
of the subject is called General Pathology. Special Pathology deals with 
the forms and details of lesions in individual organs or parts of the 
body. 

The human body is so complex in its organization that the student of 
pathology, like the student of normal morphology and i^hysiology, is 
under the constant necessity of seeking light through the study of sim- 
pler organisms. In our extremely differentiated and intimately co-ordi- 
nated cells, many features fundamentally simple are veiled or modified ; 
so that we can understand them only when we interpret them in the 
light of less advanced forms. 



68 INTRODUCTION. 

Thus it is tliat in the lore of the zoologist and the botanist we may 
find the key to obscure and important manifestations of aberrant cell 
life. It is in truth through the pursuit of Comparative Fathology that 
some of our greatest advances in the conceptions of disease have been 
won, and in it lies the brightest promise for the future. In the light of 
embryology many obscure pathological processes become plain and many 
clews to fruitful research are secured. 

Furthermore, so much depends upon the metabolism of the body in 
health and disease that it is to chemistry, both physiological and patho- 
logical, that the scientific physician looks most eagerly for the solution 
of problems which each day become more numerous and urgent. 

Finally, we are daily realizing more clearly that in those complex 
and subtle processes which we are wont to call vital, such physical fac- 
tors as molecular constitution, osmosis and diffusion, gravitation, elas- 
ticity and pressure are of the highest significance and cannot in our 
studies be wisely ignored. 



CHAPTER I. 

CHANGES IN THE CIRCULATION OF THE BLOOD. 
Hyperaemia and Anaemia. 

There are several abnoriaal conditions of the circulation which at 
death may either alter considerably or disappear altogether. Among 
the more important of these conditions are hypercemia — excess of blood 
in a part; and anaemia — deficiency of blood in a part. These and the 
conditions which lead to them will not be described in detail in this 
book, which has chiefly to do with alterations of the tissue which persist 
and may be studied after death. Tissues which have been the seat of 
temporary, and sometimes of prolonged, hypersemia, may not appear 
abnormal after death, or they may look redder than normal ; they may 
be oedematous, and more blood than usual may flow from them when 
incised. On microscopic examination the blood-vessels may be normal 
in appearance, or more or less distended with blood. Long-continued 
hyperaemia may lead to haemorrhage and transudation, to pigmentation, 
to hyperplasia of tissue, or to an atrophy of tissue through pressure, 
or even to death of tissue. 

The paleness which is characteristic of anceyiiic tissues may not be evi- 
dent after death. Anaemia may lead to no recognizable microscopic 
changes. On the other hand, if long continued it may induce atrophy 
and fatty degeneration, and, if excessive, may lead to death of tissue. 

Haemorrhage and Transudation. 

HAEMORRHAGE. 

Haemorrhage is an escape of blood from the heart or vessels. It may 
occur from a rupture of the walls of the vessels, and is then called hsem- 
orrhage by rhexis. The rupture may be occasioned by injury, by lesion 
of the walls of the vessels which renders them too weak to resist the 
blood pressure from within, or it may occur from the blood pressure in 
the thin and incompletely de^^eloped walls of new-formed vessels as in 
granulation tissue, tumors, etc. 

Under other conditions, without recognizable changes in the vessels, 
all the elements of the blood may become extravasated by passing, 
without rui3ture, through their walls. This is called haemorrhage by 
diapedesis. Such haemorrhages are usually small, but may be very ex- 
tensive. They occur in the smaller veins and capillaries, the cells and 
fluids of the blood passing out through the cement substance between the 



70 CHANGES IN THE CIKCULATION OF THE BEOOD. 

endothelial cells. Although no marked morphological changes have 
as yet been detected which explain this extravasation, it is probable 
that some change in the nutrition of the walls does occur which renders 
them more permeable. Haemorrhage by diapedesis is apt to occur as a 
result of venous congestion, or when the flow of blood in the smaller 
vessels has been suspended for some time; or it may result from the 
action of some poison, or from an injury not leading to rupture ; or it 
may occur in incompletely develoj)ed blood-vessels, in tumors and other 
new - formed tissues. 

In the extravasation of blood by diapedesis the white blood cells may 
pass through the walls of the vessels, partly at least in virtue of their 
amoeboid movements ; the red cells, on the other hand, having no power 
of spontaneous movement, are, according to Arnold, carried passively 
through the walls by minute currents of fluid which, under the changed 
condition, stream in increased force and volume through the endothelial 
cement substance into the tissue spaces outside. 

The altered condition of the blood-vessels leading to haemorrhage may 
be local or general, and in the latter case it may either be congenital, as 
in some cases of the hsemorrhagic diathesis, or it may be the result of 
a general disease, such as scurvy, purpura, etc. The presence of bacteria 
in the vessels, or of bacterial or other poisons in the blood, as in malig- 
nant endocarditis and in heemoi^hilia neonatorum, may induce changes in 
the walls of the vessels, leading to extravasation. 

Very small haemorrhages are called petecMce ; larger, diffuse accumu- 
lations of blood in the interstices of the tissues are commonly called ec- 
chymoses or suggillations. A complete infiltration of a circumscribed por- 
tion of tissue with blood is called a hcemorrhagic mfarction. A collection 
of blood in a tumor-like mass is called a hcematoma. Sometimes the ele- 
ments of the tissue into which the blood escapes are simply crowded 
apart ; sometimes, as in the brain, they are broken down. 

The extravasated blood in the tissues usually soon coagulates, al- 
though exceptionally it remains fluid for a long time. A certain num- 
ber of the white blood cells may wander into adjacent lymph vessels, or 
they may remain entangled with the red cells in the meshes of the fibrin. 
The fluid is usually soon absorbed ; the fibrin and a portion of the white 
blood cells disintegrate and are absorbed. The red blood cells soon give 
up their haemoglobin, which decomposes and may be carried away or be 
deposited either in cells or in the intercellular substance at or near the 
seat of the haemorrhage, either in the form of yellow or brown granules 
or as crystals of haematoidin. Sometimes all trace of extravasations of 
blood in the tissues disappears, but frequently their seat is indicated for a 
long time by a greater or less amount of pigment or by new-formed con- 
nective tissue. Occasionally the blood mass, in a more or less degenerated 
condition, becomes encapsulated by connective tissue, forming a cyst. 

The action of phagocytes (see page 115) in the disposal of dead ma- 
terial is here, as it is under a great variety of conditions, an important 
factor in the restoration of the body after lesion to its normal conditions. 



CHANGES IN THE CIRCULATION OF THE BLOOD. 71 

HEMORRHAGES IN THE ^N'EWBoRN. 

Hsemorrhages, sometimes extensive, in various parts of the body — 
gastro- intestinal canal, mouth, nose, navel, or the viscera — are not infre- 
quent in the first few days of life. Aside from the occasional discovery 
of ulcers in the gastro -intestinal walls, the reason for these haemorrhages 
is not evident at autopsy. This condition has been called morbus macu- 
losus neonatorum. Haemorrhages from the skin, mucous membranes, or 
navel may take place in the syphilitic new-born. Hsemogiobinuria may 
occur in epidemic form in young children. 

HAEMOPHILIA {Scemorrliagie Diathesis'). 

This abnormal condition consists in a liability to persistent haemor- 
rhage on the slightest provocation, and is dependent upon some consti- 
tutional peculiarity which is unknown to us. It is usually hereditary. 
An uncommon thinness of the intima of the arteries has been noticed in 
some cases, and other changes have been described ; but there are no con- 
stant lesions associated with the haemorrhages, as yet discovered, which 
would satisfactorily account for their occurrence. The haemorrhages may 
be traumatic in origin, or they may occur spontaneously from the mu- 
cous membranes. 

TRANSUDATION. 

Transudation is the passage, through the walls of the blood-vessels 
into the interstitial spaces outside, of fluid from the blood, with little or 
no admixture of its cellular elements. This occurs constantly, to a cer- 
tain extent, under normal conditions, and forms the commencement of 
the lymph circulation. But when the amount of fluid passing through 
the walls of the blood-vessels is increased, or its outflow into the larger 
lymph trunks is hindered so that it accumulates in undue quantity in the 
interstices and lymph channels of the tissues, the condition is pathologi- 
cal. An accumulation of transuded fluid in the interstices of the tissues 
is called oedema ; in the serous cavities, droj)sy. 

Its occurrence may depend upon some hindrance to the venous circu- 
lation or increase of capillary pressure, especially when associated with 
alterations in the walls of the blood-vessels or upon changes in osmotic 
pressure induced by a reduction in the nutrient efficiency of the blood, 
by injuries, or in other ways which may afl'ect the processes of filtration 
and osmosis, by which chiefly, it is believed, the normal transudation of 
fluids occurs. There is, furthermore, strong and increasing evidence that 
the endothelial cells of the capillaries possess active secretory or other 
functional capacities which should be taken account of in the attempt to 
comprehend transudation as well as many other pathological phenomena 
and lesions. ^ 

A simple interference with the outflow of lymph does not usually 

^ Consult for a study of lympli formation: Hmnhurger, Ziegler's Beitrage zur path. 
Anat., Bd. 14, p. 443, 1893. 



72 



CHANGES IN THE CIRCULATION OF THE BLOOD. 



alone suffice to induce transuda- 
tion, although it may favor its oc- 
currence. 

The transuded fluid, called 
transudate, is usually transparent 
and colorless or yellowish ; it con- 
tains the same salts as the blood 
plasma, but less albumin. It may 
contain fat, mucin, urea, biliary 
acids, coloring-matter of the bile ; 
fibi^inogen is usually present in 
vaiiable quantity, and, rarely, 
fibrin. It may contain endothe- 
lial cells from the lymph spaces, 
and a variable number of red and 
white blood cells. The amount of 
fluid which may accumulate in the 
tissues varies greatly, depending 
upon whether they are loose or 
dense in texture. The fibres and 
cells of loose tissues may be 
crowded widely apart; the cells 
are apt to be more granular than 
normal, they may contain droplets 
of fluid or they may be atrophied. 
Transudates occurring in inflam- 
mation usually contain a consid- 
erable number of white blood cells and more or less fibrin, and differ in 
this from the non- inflammatory transudations ; but in some cases there 
is no sharp distinction between them. The inflammatory transudates 
are often called exudations or exudates. 




Fig. 8.— Occluding Thrombus op the Iliac. 

The vessel is laid open, showing the lamellated clot. 



Thrombosis and Embolism. 

THROMBOSIS. 

Thrombosis is a coagulation of blood in the heart or vessels during 
life. The coagulum is called a thrombus. Thrombi may lie against the 
wall of the vessel, only partially filling the lumen, and are then called 
parietal thrombi^ or they may entirely fill the vessel, and are then called 
occluding thromhi (Fig. 8). 

The thrombus may form first upon the wall, and by more or less con- 
tinuous deposit of fresh material, may extend, usually but not always, in 
the direction of the blood current, either as a parietal or an occluding or 
obstructing thrombus along the vessel or into connecting channels. 

Thrombi may occur as the result of an injury to the wall of a vessel, 
or may follow its compression or dilatation ; they may result from some 
alteration of the wall of the vessel by disease or by the retardation of the 



CHANGES IN THE CIRCULATION OF THE BLOOD. 



73 



iifeSHIM 






<? 







Fig. 9.— portion of Red Thrombus. 

This shows red blood cells, flbrin, and a few 
leucocytes. 



circulation. So long as the endothelial lining of the vessels is intact, 
simple retardation of the circulation does not usually alone suffice to in- 
duce coagulation ; but changes in the en- 
dothelium, in a great variety of condi- 
tions, such as inflammation, degeneration, 
atheroma, calcification, and the presence 
of bacteria, ' tumors, and foreign bodies, 
favor its occurrence, especially when as- 
sociated with changes in the circulation 
or in the character and contents of the 
blood. Thrombosis is a not infrequent 
complication of the infectious diseases as 
well as of the cachectic conditions associ- 
ated with various acute and chronic gen- 
eral diseases. 

Thrombi may be composed of fibrin 
and of red and white blood cells, inter- 
mingled in about the same proportion as 
in an ordinary extravascular blood clot 
(Fig. 9). These are called red thrombi, 

and usually occur from some sudden stoppage of the circulation. Other 
thrombi, usually such as form while the blood is in motion, may consist 
almost entirely of white blood cells with a little fibrin, or of these inter- 
mingled with blood platelets, or they may consist almost entirely of 
blood platelets ; all of these forms are called ichite thrombi. Eed thrombi, 
when decolorized by changes in the blood pigment, may somewhat re- 
semble genuine white thrombi. Mixed thrombi are usually lamellated 
(Fig. 10) and contain varying proportions of fibrin, red and white blood 
cells, and platelets. 

After a certain amount of shrinkage by which the fluids are squeezed 
out and the thrombus becomes denser and drier, the changes which occur 
in the thrombus may be either in the direction of degeneration or organ- 
ization. The leucocytes, the fibrin, and the blood iDlates may degener- 
ate, forming a granular material which may become infiltrated with salts 
of lime, forming the so-called phleboliths, or vein stones. In other cases 
the thrombi may soften and disintegrate. This softening may be simple 
and the result of fatty or other form of tissue degeneration, resulting in 
a white or reddish or brown grumous mass, which may resemble, but is 
not, pus. Or, it may be associated with bacteria or other infectious ma- 
terial with genuine suppuration. In this ^^ purulent^' or ^^ septic ^^ soft- 
ening of the thrombus the risk is great of a distribution of the infectious 
material through the circulation. Finally, the thrombus may be replaced 
by a new formation of vascular connective tissue, itself disappearing as 
the new tissue is formed. This is called '' organization of the thrombus, ^^ 



^ For a study of the role of micro organisms in the formation of venous thrombi see 
Jakoicski, Cbl, 1 Bak., Abth. I., Bd. 28, p. 801, 1900, Bibl. Consult also Welch on in- 
fective thrombi, Albutt's "System of Medicine," vol. vi., p. 169. 



74 



CHANGES IN THE CIRCULATION OF THE BLOOD. 



but in reality the new connective tissue is produced, not from the cells 
of the thrombus itself, but from the cells of the walls of the affected 



/' 



Fig. 10.— Lamkllated Thrombus. 

This is an occluding thrombus. At the right and also above are masses of red blood cells, while the re- 
mainder is largely fibrin in layers, indicating successive deposits. 

trunk, from whose vessels the new blood-vessels of the thrombus also 
arise (compare page 104). In this way the vessel may be completely 



\ 



Fig. 11.- Organized Thrombus. 

This shows the vascular connective tissue which has replaced the clot, with five new channels through 
which the circulation is re-established. 



CHANGES IIS" THE CIRCULATION OF THE BLOOD. 



75 



and permanently occluded, or, more rarely, one or several channels may 
be established through the new connective-tissue mass (Fig. 11). 

Thrombi in veins may lead to hypersemia and oedema ; in arteries, to 
an anaemia whose significance will vary greatly, 
depending upon the situation of the occluded 
vessel. ' 

Hyalin T hi^ombi,— JJndev a variety of con- 
ditions, but especially in local and general in- 
fections and in intoxications, there is present 
in the capillaries and in the small arteries and 
veins a homogeneous, translucent, nearly color- 
less material, partially or wholly blocking the 
vessels. This hyalin material, whose origin is 
still in doubt, has in general a staining reac- 
tion similar to fibrin. 

EMBOLISM. 



Embolism is the stoppage of a blood-vessel 
by the arrest in its lumen of some material car- 
ried along in the circulating blood. The mass 
causing the stoppage is called an embolus (Fig: 
12). This may be composed of a great variety 
of substances. The most common emboli are 
detached portions of thrombi, and these may 
have all the variety of structure which thrombi 

present. Masses 




Fig. 12.— An Embolus Lodged 
AT THE Point of Division of an 
Artery. 

This is a portion of clot which has 
been detached from a point above 
and swept along the blood current. 
It has increased in length by coagu- 
lation at its free extremities. 



'•# 



of bacteria or other 
parasites, fragments of the heart valves 
and of tumors, droplets of fat from the 
medulla of fractured bones (Fig. 13), 
parenchyma cells, "" masses of pigment, 
bubbles of air, etc., may form emboli. 
Embolism is, in a majority of cases, 
confined to the arteries and to the 
branches of the portal vein. 

The primary effect of the stoppage 
of an arterial trunk is, of course, largely 
to deprive the region of the body to 
which its branches are distributed of its normal supply of blood. If 

^ For a thorough and admirable consideration of the subject of thrombosis and em- 
bolism with bibliography, consult WelcJi, Albutt's "System of Medicine," vol. vi., p. 
155 et seq. 

'^ The presence of liver-cell emboli in the lung capillaries and in the heart clots after 
traumatic rupture of the liver, and in infectious diseases involving local necroses of the 
liver has been described by various observers. Emboli believed to be composed largely 
of placental cells or of cells from the bone marrow are also described under various con- 
ditions. The facts relating to this subject of parenchyma-cell emboli and its alleged 
significance may be found summarized by Lvbarsch, Fortschritte der Medizin, Bd. xi. , 
pp. 805 and 845, 1893; and by Aschoff,Yir chow's Archiv, Bd. cxxxiv., p. 11, 1893. 
Consult also Warthin, The Medical News, September 15th, 1900, Bibl 



13.— Fat Emboli in the Blood Ves- 
sels of the Lung. 
This followed bone fracture. 



- f 



76 CHA^^GES IN THE CIECULATION OF THE BLOOD. 

the branches of the occluded artery form anastomoses with other arteries 
beyond the point of stoppage, a collateral circulation may be estab- 
lished and the embolus do no harm. If, however, the occluded vessel 
be a so-called terminal artery — that is, one whose branches do not form 
anastomoses with other arteries — the result of the embolism is quite 
different. When a terminal artery is occluded by an embolus, the tissue 
of the affected region usually dies, and there may be 
/^^ an extravasation of blood by diapedesis, leading to the 

, ' . formation of a dark-red, solidified area, called a lioem- 

orrliagic infarction^ The area of infarction corre- 
sponds to the region supplied with blood by the 
occluded vessel, and is usually more or less wedge- 
\ shaped (Fig. 14). 

; After a time the infarction becomes decolorized, 

inflammatory changes may occur in its periphery, the 
blood and involved tissues may undergo degeneration 
and be absorbed, and, finally the seat of the infarction 
may be indicated only by a mass of cicatricial tissue, 
which frequently contains more or less pigment. 

In another class of cases, instead of an extravasa- 
tion of blood in the affected region, the tissue is sim- 
ply deprived of nourishment and undergoes necrosis. 
The affected area is then usually light in color and 
is called a ivMte infarction. Inflammatory changes may 
occur in its periphery and a new connective -tissue 
capsule form around it, and the dead mass may thus 
persist for some time, or be gradually absorbed and 
replaced by cicatricial tissue. The scope of this book does not permit 
us to consider the somewhat complicated and often obscure reasons why 
in one case there is hsemorrhagic, in another white infarction, as a 
result of embolus. 

If the embolic material consists of or contains infectious substances, 
such as some forms of bacteria, in addition to the mechanical effects of 
simple emboli, we may have gangrene, suppuration, formation of ab- 
scesses, etc., as the result of the local action of the infectious mate- 
rial, even though this may be present in very small amount. 

The organs in which embolic infarctions most frequently occur are 
the spleen, kidney, brain, lungs ; less frequently the heart, retina, liver, 

^ When an embolus lodges in a terminal artery, and the circulation in the territory 
supplied by its branches ceases, the pressure from the side of the artery is reduced to 
zero ; but, on the other hand, according, to Cohnheim, the venous pressure now makes 
itself felt in a backward direction, and the capillaries and small veins in the affected 
region become crowded with blood. This blood is stagnant, however, and the walls 
of the small vessels, being deprived of their usual nourishment, undergo, it is believed, 
degenerative changes which favor the occurrence of extensive diapedesis. Thus in 
the htemorrhagic infarction not only the blood-vessels, but the extravascular tissues also, 
are crowded with stagnant blood. The researches of Litten make it seem probable that, 
in most cases, the back pressure in the region of infarction comes, not from the veins, 
or not from them alone, but from adjacent arterial twigs which communicate Avith the 
capillaries of the affected region. 



r 


» -.. ' 


,<- -^ 




\ V 


\4 


i , 


/ 

1 


lJ-^ 




IG. 14.- 


Infarctions 


OF THE Spleen. 



CHANGES IN THE CIRCULATION OF THE BLOOD. 77 

and small intestines. Hsemorrliagic infarctions are not liable to occur in 
the liver from emboli in the branches of the portal vein, on account of 
the blood supply which may come to the affected region through the 
branches of the hepatic artery. On the other hand, embolic abscesses 
from infectious emboli are of not infrequent occurrence here. Hsemor- 
rhagic infarctions may occur exceptionally, in regions not furnished with 
terminal arteries, as in the small intestines. 

Cases of aberrant embolism are recorded in which venous emboli have 
passed through an open foramen ovale into the arterial system. 

Eetrograde transportation of venous emboli has been several times 
recorded. 



CHAPTER II. 

ATROPHY, DEGENERATION, PIGMENTATION, AND 

NECROSIS. 

General Considerations. 

There are three phases of activity in the transformations of energy 
which are characteristic of living cells. These are nutrition, reproduc- 
tion, and functional activity. But while these manifestations of energy 
are more or less distinct as properties of living matter, they are closely 
interdependent. It is the suitable balance of these activities fixed by a 
prolonged environment which determines what we call health. When 
this balance is disturbed beyond the limits of physiological variation, the 
alterations which result may be manifest, either in the diminution or de- 
struction of tissue, or in its increase or new formation. In other words, 
the cells of the body when placed under conditions which seriously in- 
terfere with the orderly transformations of energy may undergo altera- 
tions from the normal which are retrogressive on the one hand, or pro- 
gressive on the other. 

It is well to remember that retrogressive as well as progressive 
changes in the body are not limited to pathological conditions but form 
a part of the normal processes through which growth is secured and 
function maintained.^ 

We shall in this chapter consider the retrogressive processes and their 
effects ; in the next those which are progressive. 

Atrophy. 

Atrophy is a diminution in the size of the body, of organs, or of tissue 
elements. It occurs as a physiological process in man as well as in cer- 
tain of the lower animals. Thus in man the thymus and the umbilical 
vessels undergo atrophy at an early period ; while in old age atrophy of 
the sexual organs and of the tissues in general is the usual mark of senil- 
ity. ' On the other hand, as a pathological process, atrophy may occur 
in connection with disturbances of innervation or nutrition ; from disuse 
or from pressure ; or from the presence of poisons. Although it is con- 
venient to name these as phases of atrophy, they are not fundamentally 

^ For a resume of the relationship between normal and pathological retrogressive 
processes see Minot, Middleton Goldsmith Lecture on "The Embryological Basis of 
Pathology," Science, March 29th, 1901. 

2 For a study of the changes in the body in development and senility see the mono- 
graph of Muhlmaiin, Wiesbaden, 1900, Bibl. 



ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 



79 



distinct. In simple atrophy, under whatever conditions it may occur, the 
tissue elements become smaller without marked alterations in structure, 
and may finally disappear altogether. In the majority of cases, how- 
ever, atrophy of cells or other tissue elements is not simple but is asso- 
ciated with, and often determined by, various phases of degeneration — 
degenerative atrophy. 

Degeneration. 

ALBUMINOUS DEGENERATION (Cloudy Swelling, Parenchymatous De- 
generation, Acute Degeneration, Granular Degeneration). 

Under a variety of conditions in which there is a disturbance of tis- 
sue nutrition, but especially often in infectious diseases and in intoxica- 
tions when poisonous substances come in contact with the tissues, the 




Fig. 15.— Albuminous Degeneration.— Kidney. 
The lesion is moderate in degree and is most marked in the largest tubule ahove. 



cells of the body show an accumulation in the cytoplasm of albuminous 
granules, of various sizes and forms. This is a type of cell degeneration 
which is so often associated with infectious diseases and certain phases 
of inflammation, that it is sometimes regarded as a part of the inflam- 
matory process. The cells in this condition are usually swollen and are 
more opaque than normal, the nucleus being somewhat concealed in the 
granules when these are numerous (Fig. 15). The albuminous granules 
in the cells are soluble in dilute acetic acid but not in ether, being thus 
distinguished from fat. 

\\Tiile all the cells of the body are subject to this phase of proto- 
plasmic degeneration, it is most pronounced and frequent in the paren- 
chyma cells of the liver and kidney, in muscle, in epithelial cells of the 
mucous membranes. These are, it will be seen, cells in which metabolism 
is active and the exigencies of nutrition are imperative. The alterations in 
the ganglion cells of the central nervous system in infectious diseases and 



80 ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 

ill various forms of intoxication are somewhat different from those oc- 
curring in other parenchyma cells and will be described in the section 
devoted to the Brain and Spinal Cord. 

Cells in a condition of albuminous degeneration may return to their 
normal state, they may become fatty or they may die, become necrotic 
and disintegrate. 

The liver, kidney, muscle, mucous membranes, etc., when in this con- 
dition, are often swollen and in gross appearance more opaque and gray 
than when normal. 

The exact chemical nature of this degenerative process is obscure 
and will doubtless remain so until we know much more than we now 
do of cell structure and cell metabolism. 

Technique. — The microscopical study of this lesion is best made in fresh frozen 
sections of the tissue, by the rapid formahn method, page 52 ; or in fresh tissue teased 
in one-half-per-cent salt solution. 

FATTY DEGENERATION AND FATTY INFILTRATION. 

It is customary and convenient in considering the abnormal accumu- 
lation of fat in the tissues to assume that in one set of cases — fatty de- 
generation — the fat is formed by a retrograde metamorphosis or degen- 
eration of the proteid elements of protoplasm, a i^rocess by which the 
integrity and capacity of the cell are compromised; while in the other — 
fatty infiltration — it may be due to a simple accumulation in the cell of 
fat formed elsewhere — a condition of less significance. 

The validity of this assumption has of late been called in question. 
It involves in large measure the solution of the physiological problem 
whether normally the fat in the body is formed from proteids or from 
carbohydrates. Concerning this many experiments and much argument 
have been made ' ; but it appears not yet to be solved. The traditional 
distinction between fatty degeneration and fatty infiltration will there- 
fore be made here, with such modification and reserve as are fitting in 
view of our lack of knowledge. 

Fatty Degeneration. 

In fatty degeneration there is an accumulation of larger and smaller 
droplets of fat in the cell, sometimes so slight as to be scarcely visible, 
sometimes so great as largely to replace the protoplasm, crowding the 
nucleus to one side. These strongly retractile fat droplets are not 
changed by dilute acetic acid. They are soluble in ether, and when fresh 
are stained black by osmic acid (Fig. 16). ^N^ot infrequently, feathery 
clusters of delicate fat crystals are present in the cells. Cells in exces- 
sive fatty degeneration may disintegrate, forming an oily detritus in 
which, especially when much moisture is present, cholesterin crystals 
may form by decomposition of the fat. 

^ For a critical summary of this question, see Taylor, American Journal of the Med- 
ical Sciences, vol. cxvii., p. 569, 1899. 



ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 



81 



To the naked eye, organs in a condition of marked fatty degeneration 
are usually larger and softer than normal, have a grayish -yellow color or 
are mottled with yellowish streaks or patches, and the normal markings 
of cut surfaces are more or less obscured. 

Fatty degeneration may be associated with or may follow albuminous 
degeneration and may occur under similar general conditions. It may 



"^WS^""% 




::, : $ 



c» *%*^ ft f' *> 



Fig. 16.— Fatty Degeneration- Kidney. 
The fat droplets are stained black by osmic acid. 



be due to local or general disturbances of nutrition, from a great variety 
of causes — disturbances which either directly affect the life processes of 
the cells themselves, or which produce alterations in their nutritive sui3- 
ply. In addition to its local occurrence, as a result of local disturbances 
of circulation in the vicinity of inflammations or in tumors, etc., it is 
apt to occur in the liver, heart muscle, and kidney in chronic exhausting 
diseases and in conditions and diseases to which profound anaemia is in- 
cident, or as the result of the action of certain poisons, such as phos- 
phorus and arsenic. 

Fatty Infiltration. 

This is of common occurrence under normal as well as pathological 
conditions. The fat is believed to originate outside of the cells, accumu- 
lating in them, and inducing a pass- 
ive atrophy of the cytoplasm. Cells 
in a condition of abnormal fatty 
infiltration are scarcely to be distin- 
guished morphologically from those 
involved in fatty degeneration. The 
presence in the cells of large or small 
droplets of fat without marks of de- 
generation in the remaining proto- 
plasm has been regarded as distinct- 
ive of infiltration (Fig. 17). 

In some phases of fatty infiltra- 
tion, as in the heart (Fig. 401) or the 
pancreas, for example, the fat accu- 
mulates in the cells of the interstitial 
6 




■v^-Q 



Fig. 17.— Fatty Infiltration op Liver Cells. 

In two of the cells the nucleus is crowded to one 
side by the accumulated fat. 



82 



ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 



connective tissue in a manner identical with that in which the normal 
panniculus adiposus is formed. The heart muscle or the gland cells are, 
under such conditions, affected secondarily through pressure atrophy 
from the accumulated fat. ' 

It should be remembered that fatty infiltration and fatty degeneration 
may occur simultaneously. 

Technique. — Tissues in a condition of fatty degeneration or infiltration may be 
teased fresh in salt solution; or they may be hardened in Flemming's osmic-acid solu- 
tion, see page 53, in preparation for sectioning. Hardening in Orth's fluid and after- 
ward in alcohol gives moderately good results if the lesion be extensive. But it should 
be remembered that in tissues which have been soaked in alcohol the fat is no longer 
present, its former seat being indicated by clear spaces which are filled with the mount- 
ing medium. The fat crystals, however, often persist after prolonged soaking in alcohol. 



AMYLOID DEGENERATION (Waxy or Lardaceous Degeneration). 

This is a process by which the basement substance of various forms 
of connective tissue, and especially the walls of the blood-vessels, be- 
come swollen and thickened by their conversion into a translucent, firm, 

glassy, colorless material, albuminous 
in character. This albuminous ma- 
terial may be present in the tissues in 
such small amount as to be recogniz- 
able only under the microscope, or 
it may be so abundant as to give a 
very characteristic appearance to the 
tissue. Parts in which the lesion is 
marked are usually larger and contain 
less blood and feel harder than nor- 
mal, and have a peculiar shining and 
translucent appearance which varies 
in character, depending upon the ex- 
tent and distribution of the degener- 
ated areas and upon its association 
with other lesions, such as fatty 
degene^'ation. It most frequently 
occurs in the smaller arteries and 
capillaries (Fig- 18), whose lumen is 
encroached upon by the thickening 
of the walls which the process in- 
volves. It is usually the media and intermediary layers of the intima 
which are earliest and most extensively affected. The change also often 
occurs in the interstitial connective tissue and membranse proprise of 
organs and in reticular connective tissue. It is I'Oth asserted and denied 
that it may affect the parenchyma cells of orga is. We have not been 
able to find unmistakable evidence of its occurrence in parenchyma 

^ For a study of the deposition of fat in cells, see Arnol.i, Virch. Arch., Bd. 163. p. 
1, 1901. 




Fig. 18.— Amyloid Degeneration of Capil 
laries of a glomerulus in the kidney. 

A, Waxy capillaries stained red ; B, normal capil 
lanes. 



ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 



83 



cells. These, however, frequently undergo atrophy as the result of 
pressure from the swollen, degenerated tissue. 

It is not yet known whether amyloid degeneration is due to a direct 
transformation of the tissue, or is an infiltration of the tissue by some 
abnormal material formed elsewhere and brought to it, or is derived from 
the blood. 

Amyloid degeneration occurs most frequently and abundantly in 
the liver, spleen, kidneys, intestinal canal, and lymph nodes ; but it may 
occur, usually in a less marked degree, in other parts of the body : in 
the larger blood-vessels, in the interstitial tissue of the heart and mucous 
membranes of the air i)assages, and in the generative organs. It may 
occur locally or appear in various parts of the body at once. It most 
frequently occurs in connection with severe wasting diseases, particu- 
larly in those involving chronic sux)puration and ulceration, especially of 
the bones. It is common in tuberculosis, syphilis, in the cachectic con- 
dition induced by malignant tumors, and is occasionally seen in severe 
malarial infection, dysentery, and leukaemia. ^ 

Technique. — For microscopical examination the tissue, either fresh or after pres- 
ervation, should be cut into thin sections, and these deeply stained with one-per-cent 
aqueous solution of methyl violet ; the sections are washed in water and mounted in 
glycerin. The differentiation between the amyloid and other parts is more distinct if, 
after staining, the specimen be dipped for an instant in HCl and alcohol 1 : 100, and then 
carefully rinsed, before mounting in glycerin. The degenerated areas are thus stained 
rose-red (Fig. 18), while the normal tissue elements have a bluish-violet color. In some 
cases, for reasons which we do not know, the amyloid substance does not show a well- 
marked reaction with methyl violet. For the de- 
tection of amyloid in fresh tissues by the iodine 
reaction see p. 28. 



Coi^pora Amylacea are small, spheroidal, 
homogeneous or lamellated bodies (Fig. 
19), which assume a bluish color on treat- 
ment with solution of iodine or iodine and 
sulphuric acid. They are frequently found 
in the acini of the prostate gland, some- 
times in large numbers; in the ependyma 
of the brain and cord; also in extravasa- 
tions of blood and in various other situa- 
tions. They may occur under normal as well as pathological conditions, 
and are apparently of little importance. They seem to have nothing to 
do with amyloid degeneration, although they somewhat resemble its 
products. Some of the tube casts of the kidney resemble in many 
respects the corjiora amylacea. ^ 

' An extended studv of amyloid degeneration may be found in a monograph by 
Wichmann, Ziegler's Beitrage, Bd. 13, p. 487, 1893. 

A later bibliography with a summarj- of experiments on the production of amyloid 
degeneration in animals Avill be found in an article h\ Maximoic, Virch. Arch., Bd. cliii., 
p. 353, 1898. 

- For a study of the relationship of corpora amjiacea to amyloid substances, see 
Ophuls, .Jour. Exp. Med., vol. v., p. Ill, 1900, Bibl. 




FiCr. 19.— Corpora Amylacea. 
From prostate gland. 



84 



ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 



GLYCOGEN INFILTRATION. 

Glycogen appears under abnormal conditions in the cells as hyalin, 
mostly globular masses of varying size (Fig. 20). It is soluble in water, 

is stained brownish-red by iodine, and 

^*^. does not assume a greenish color by the 

/ .^^ further addition of sulphuric acid. In 

diabetes it may occur in large quantities 
in the liver cells and in the epithelial 
cells of the uriniferous tubules, especially 
in those of Henle's loop (Fig. 331) and 
in leucocytes. It may be found in fresh 
pus cells, in the cells of various forms of 
tumors, and in leucocytes in the blood in 
leukaemia, in chronic diseases of the 
gastro-intestinal tract in children, and in various chronic diseases. 






Fig. 30.— Glycogen Infiltration 
thelium of kidney. 

The glycogen droplets are unstained. 



Epi- 



Tecitnique. — If the tissue to be examined for glycogen be fresh, the iodine should 
be used in solution in glycerin (equal parts of Lugol's solution and glycerin), in order 
to avoid its solution. If specimens are to be hardened, this should be done in absolute 
alcohol to avoid the solution of the glycogen. Sections may be stained with picro-acid 
fuchsin (Van Gieson's stain) or with a dilute solution of iodine in alcohol (tincture 
iodine 1 part, absolute alcohol 4 parts), cleared up and studied in oil of origanum. 

SEROUS INFILTRATION OF CELLS (Hydropic Degeneration, 

Vac uolization) . 

Under many pathological conditions, cells, especially those of mucous 
membranes, glands, muscles, tumors, etc., contain one or more larger or 
smaller droplets of clear fluid (Fig. 21). The cell may thus be distended. 



-^ 




Fig. 31.— Serous Infiltration 
OF Epithelial Cells. 




Fig. 22. — Mucous Degeneration of Epithelial 
Cells. 

From a cyst-adenoma of the ovary. 



These droplets are usually extra-nuclear and may crowd the nucleus to 
one side of the cell. The nature and source of this accumulated fluid are 
not known. Its transparent appearance in the granular protoplasm has 
given rise to the term ^^ vacuole.^' It may be associated with general 
tissue oedema, with inflammatory and degenerative processes, etc. 



ATROPHY, DEGENEKATION^, PIGMENTATION, AND NECROSIS. 85 

MUCOUS DEGENERATION. 

Mucous degeneration may occur in cells or in intercellular substance. 
AVTien occurring in cells it consists, under pathological as under normal 
conditions, of the transformation of the protoplasm into a translucent, 
semi-fluid material, occupying more space than the unaltered protoplasm, 
and hence causing a swelling of the cells (Fig. 22). This new-formed 
material contains mucin in solution, which is precipitated by acetic acid. 
It occurs under a A^ariety of conditions, sometimes as an abnormal in- 
crease of a normal function of cells, as in many catarrhs, sometimes as 
an entirely abnormal transformation. The cells may be totally destroyed 
by the accumulation of the mucoid material within them. 

In certain cases, as in many tumors, in cartilage, bone, and other tis- 
sues, the intercellular substance may undergo conversion into mucin-con- 




Fifi. 33.— Mucous Degeneration of Fibrous Tissue of MammA. 

taining material, losing almost entirely its original structure (Fig. 23). 
The cells in such cases may be affected only secondarily by the pressure 
which the new-formed material exerts upon them. 

Technique. — Tissues should be hardened in Ortli's fluid or formalin, followed b}^ 
alcohol ; the sections are stained with picro-acid fuchsin or with haematoxylin, which 
colors the mucin-containing portions. 

COLLOID DEGENERATION. 

This is very closely allied, both in chemical and morphological char- 
acters, to mucous degeneration, and in many cases there is no definite 
microscopic distinction between them. But colloid material, which is 
normally present in the thyroid, is firmer and more consistent than mu- 
cous, does not yield a precipitate on addition of acetic acid or alcohol, 
and its formation is usually confined to cells ; not involving intercellular 
substance, except by an atrophy which its accumulation sometimes in- 
duces. The cells may contain larger and smaller droplets of colloid ma- 
terial, or the latter may nearly or entirely replace the protoplasm and 
accumulate to such an extent as to cause rupture and destruction of the 



86 



ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 




cell. In this way, aud by the atrophy of intercellular substance which 
its accumulation causes, cysts may be formed containing colloid material 
and cell detritus. Colloid degeneration is of most frequent occurrence in 
the thyroid gland. A material resembling, if not identical with, colloid 
is occasionally seen in the form of homogeneous globules in the tubules of 
kidneys which are the seat of other lesions, in the hypophysis, and in 
various tumors. 

Technique. — Tissues should be hardened iu formalin, or Orth's fluid, and stained 
with picro-acid fuchsin. 

HYALIN DEGENERATION. 

This is the transformation of tissues into a transparent, glassy sub- 
stance, much resembling amyloid in its morphological characters (Fig. 
24) ; but it does not give the micro -chemical reactions of amyloid, and 

appears under different conditions. 
Hyalin substance is resistant to the 
action of acids, and stains readily 
with acid fuchsin and eosin. It 
occurs especially in the walls of the 
smaller blood-vessels in various 
parts of the body, in voluntary 
muscle fibres, and is said sometimes 
to involve interstitial tissue. It 
has been described as occurring 
in the brain, lymj^h nodes, and ova- 
ries ; in the tubules of the kidney, 
in the walls of aneurisms, in muscle fibres, in the lesions of diphtheria, 
tuberculosis, and syphilis, in the hyaloid membrane and vessels of the 
eye, and elsewhere. It is believed by some observers that fibrin, blood 
plates, and leucocytes may undergo hyalin degeneration, and in the form 
of the so-called hyalin thrombi this substance may block the capillaries 
in many infectious diseases — typhoid fever, pneumonia, diphtheria, pyae- 
mia, etc. — and under a variety of other conditions. Hyalin degeneration 
seems to be, in some ways, allied to coagulation necrosis, but its exact 
significance and relations to other forms of degeneration, and the con- 
ditions of its occurrence, are not yet known. There are probably A^ari- 
ous substances occurring under many different conditions, which we now 
call hyalin and whose relationship to each other and to amyloid, mucoid, 
and colloid material is little understood. ' 

Technique. — Hardening in alcohol, Orth's fluid, or formalin. Staining by picro- 
acid fuchsin, or by haematoxylin and eosin. 

CALCAREOUS INFILTRATION. 

There is in this condition a deposition, either in cells or in the inter- 
cellular substance, of larger and smaller granules composed chiefly of 

' Consult for bibliography of studies on hyalin degenei-ation Luharsch and Ostertag's 
"Ergebnisse der allg. path. Morphologic und Physiologic," etc., Jahrg. i., Abth. i., 
1895, p. 201. 



Fig. 24.— Hyalin Degeneration in the Walls of 

Small Blood- Vessels. 

From a Sarcoma. 



ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 87 

phosphate and carbonate of calcium. These particles, when abundant, 
give hardness, brittleness, and a whitish appearance to the affected tis- 
sue. Under the microscope they appear dark by transmitted, white and 
glistening by reflected, light. Tissues may be nearly comj)letely per- 
meated with salts, or the latter may be scattered in patches through 
them. Sometimes large lamellated concretions are formed in tissues, 
usually at the seat of some old inflammatory process. Calcification usu- 
ally occurs in parts of tissues which are dead or are in a condition of 
reduced vitality as a result of some antecedent abnormal process, as a rule 
of an inflammatory nature. Among the most common and important 
examples of calcareous degeneration may be mentioned those which occur 
in the valves of the heart and walls of the blood-vessels. 

Technique. — The carbonate of lime deposited in the tissues is dissolved by dilute 
acids with evolution of carbonic acid gas. This process may be observed under the 
microscope by running five-per-cent. hydrochloric acid under the cover glass upon 
unstained sections; the gas bubbles are caught as they evolve beneath the cover. 

Those parts of tissues which are in an early stage of calcification, as well as those 
from which the lime has been removed by acids, are usually stained an intense blue by 
hsematoxylin. 

Pigmentation. 

There is under normal conditions a certain amount of pigment in the 
body — in the rete Malpighi of the skin, in the eye, in muscle, and in 
fat. This pigment is elaborated by the body cells and may vary consid- 
erably in amount. 

The pigment which is formed under pathological conditions may be 
derived from the blood — hcematogenous ; from the bile — hepatogenous ; or 
it may be elaborated by various cells after the analogy of the normal 
pigment — metabolic. Finally, pigment may be introduced into the body 
from without by drugs, in tattooing, or by inhalation. The pigment in 
the body, of whatever origin, may be in yellow, brown, black, or reddish 
granules, or in crystalline form. It is often deposited in cells, but may 
lie free in the intercellular substance. 

HEMATOGENOUS PIGMENT. — Blood pigment may form by the decom- 
position of haemoglobin in thrombi or in extravasated blood. Under 
these conditions, the haemoglobin which is loosely associated with the 
plasm of the red blood cells, readily diffuses, leaving the cells — so-called 
''blood shadows^' — pale and almost invisible and prone to disintegrate. 
This destruction of blood cells is called hcemolysis. Haemoglobin in solu- 
tion in the body fluids undergoes various phases of decomposition which 
we cannot follow in detail here. One of the derivatives of the haemo- 
globin is called hcemosiderin. This pigment gives the micro -chemical re- 
action for iron, ^ while certain further decomposition products, hwma- 

^ To differentiate iron-containing pigment in tissues, sections may be placed for an 
hour in a mixture consisting of equal parts of a two-per-cent solution of potassium 
ferrocyanide and two-per-cent solution of hydrochloric acid diluted with ninety-nine 
parts of water. The iron-containing granules under these conditions become green or 
bluish-green. 



88 ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 

toidin, for example, in amorphous or crystalline form, do not. Eed blood 
corpuscles may be taken up by various forms of phagocytes, and within 
these cells the decomposition of the hgemoglobin may lead to their pig- 
mentation. On the other hand, haemolysis may take place in the circu- 
lating blood in many forms of poisoning, in acute infections, notably in 
malaria, in pernicious anaemia, in various cachexise, etc. The haemo- 
globin thus set free in the body fluids may be eliminated or it may un- 
dergo decomposition, and its derivatives may be deposited in the tissues 
as pigment granules. 

A condition called hcemocliromatosis has been described, in which a 
brown pigment probably derived from the haemoglobin of the blood is 
deposited in various tissues of the body. The organs in this condition 
may apjDcar notably pigmented on gross examination. The pigment 
particles which are found in the epithelial cells of glands, especially of 
the liver and pancreas, contain iron ; while an iron-free pigment may be 
present in the smooth muscle cells of the gastro-intestinal canal and of 
the blood and lymph vessels, and in connective-tissue cells. This pig- 
mentation is commonly associated with cirrhosis of the liver. Haemo- 
chromatosis may be associated with diabetes mellitus and cirrhosis of the 
liver, together with pigmentation of the skin — ^'bronze skin.'^ The con- 
ditions leading to haemochromatosis are still obscure. ' 

Hepatogenous Pigment. — Pigmentation of tissues from the bile 
occurs under various conditions. The bile may enter the blood and tis- 
sue fluids in obstruction of the gall ducts by inflammation, tumors, cal- 
culi, etc. In the condition called jaundice or icterus the tissues are 
stained yellowish or yellowish-green by bile pigment. Icterus may also 
occur in infectious diseases and in toxaemia, under conditions which lead 
to destruction of red blood cells within the vessels. Bile pigment may 
be deposited in the liver and elsewhere in the form of yellow or brown 
granules. 

Metabolic Pigment. — Pigment maybe elaborated by various forms 
of cells by processes apparently somewhat analogous with those con- 
cerned in normal pigmentation.'' This is exemplified in melanotic 
tumors, most frequently of the choroid and the skin, and possibly in the 
bronze skin of Addison's disease. 

Pigment whose nature is not very clearly defined may form in the 
smooth muscle tissue of the gastro-intestinal walls, in various cachexiae, 
in the heart muscle, in the so-called ^^ brown atrophy, ^^ and, under certain 
conditions, in the liver. 

As examples of pigment introduced into the body from without, we 
may mention the deposition of minute particles of silver from the inter- 
nal use of silver salts — argyria ; the coloring of the skin and lymph 
glands from tattooing ; and especially the pigmentation of the lungs and 

' For a careful study of licemocliromatosis, with bibliography, see Ojne, Jour. Exp, 
Med., vol. iv., p. 279. 

^ For a study of the nature of skin pigment, consult Ahel and Davis, Journal of 
Experimental Medicine, vol. i., p. 361, 1896; also Chittenden and Albro, American 
Journal of Physiology, vol. ii., p. 291. 



ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 



89 



bronchial glands from the inhalation of coal and other dust — pneumono- 
koniosis (Fig. 25). This is universally present under the conditions of 










>v 



? 4 






::,,^ ^.'— :-r<^ - ^V'^.'^'^.lf^j'^o- 



Fig. 25.— Pigmentation of Connective-tissue Cells of the Lungs. 
From inbaled coal dust— anthracosis. 

indoor life which modern civilization imposes. Such pigment may be 
brown or black, and is usually in very small particles within cells or in 
the intercellular stroma. 



Necrosis. 

N^ecrosis is the death of a circumscribed portion of tissue. It may 
be the result of insufficient nutrition, from the cutting off of the blood 
supply; or it may depend upon the action of destructive chemical 
agents, extreme degrees of temperature, certain materials produced by 




Fig. 



Necrosis of Epithelium in the Kidney. 



The cells In the lower portion of the cut are nearly normal ; most of those above are more coarsely granu- 
lar and have failed to take the nuclear stain, while at the top they are disintegrating. 

the life processes of some forms of bacteria ; or it may be due to me- 
chanical injury. The general appearance of dead tissues varies greatly. 
In some cases there is a simple and gradual disintegration and softening 



90 ATROPHY, DEGrENERATION, PIGMENTATION, AND NECROSIS. 

of the tissue, resulting in a mass of degenerated cells and cell detritus, 
with more or less fluid and various chemical substances arising from de- 
composition. The softening of the brain in embolism is an example of 
simple necrotic softening. In some cases the dead tissues merely grad- 
ually dry and shrivel and become hard and dark colored. 

In another class of cases the dead tissues are permeated by fluids 
which may be dark red in color, from the solution of coloring matter 
from the blood, and may contain bacteria which induce putrefaction, with 
the production of gases and various new chemical substances. The tissues 
become swollen and granular, and disintegrate; and finally the whole 
may form a mass of irregular granules, with fat droplets, tyrosin, leucin, 
and various forms of crystals, shreds of the more resistant kinds of tis- 
sue, and bacteria. 

There is at first no evident morphological difference between dead 
cells and living cells. But very soon in the former, secondary changes 
occur. The cytoplasm becomes more coarsely granular. The nucleus 
stains less deeply or not at all with hsematoxylin or other nuclear 
dyes (Fig. 26), owing to the disappearance of the chromatin which 
seems to dissolve in the tissue juices; this is called Mryolysis. Some- 
times, however, the chromatin only partially disappears, the remainder 
breaking up into irregular, more or less deeply staining granules. This 
is called Mryorrhexis. Presently the cell body may contain fat droplets, 
or without this it may disintegrate. 

Gangrene. — When death of a considerable mass of tissue occurs, and 
this either dries, as is possible on the surface of the body, or is associated 
with putrefaction in the tissue, the condition is called gangrene. The 
involved part, when on the surface of the body, may dry and become 
hard and brown or black — mummification, or dry gangrene. ' On the other 
hand it may, when putrefactive bacteria are present, in addition to its 
discoloration, become soft and infiltrated with foul-smelling gases— wjois^ 
gangrene. If the affected part be comparatively bloodless, the discolor- 
ation, which is largely due to decomposition of the blood pigment, may 
be absent. 

Focal I^ecrosis. — Necrosis involving a small circumscribed area of 
tissue, such as is frequent in toxsemia, is called /oca? necrosis, p. 178. 

Ulceration. — Necrosis with erosion involving the surface of the 
skin or of the mucous or serous membranes is called an nicer. An ulcer 
may be necrotic in origin, from the cutting off of nutrition in a circum- 
scribed area, as in some forms of gastric ulcer. This may be associated 
with reactive inflammatory processes which tend to promote repair. On 
the other hand, the process may be inflammatory in origin, death of tis- 
sue following. 

Coagulation :N'ecrosis. — If dead areas of tissue (whether this con- 
dition be due to mechanical injury, to disturbances of nutrition, or to 
the local action of bacterial or other poisons) contain the substances 

^For a study of senile gangrene see Falta, Zeitschr. f. Heilkunde, Bd. xx., p. 393, 
1899, Bibl. 



ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 



91 






Fig. 27.— Coagulation 
Cells. 



© 



Necrosis in 



The disappearance of the chromatin 
from the nuclei is indicated by their fail- 
ure to stain, especially marked in the up- 
per cells. 



necessary for the coagulation of their albuminous constituents, or if they 
be bathed with body fluids from adjacent parts in which the circulation 

is maintained, a characteristic coagulation 
of the necrotic elements is apt to occur. 
The composition of the cells of the tissue 
is altered, so that the cell bodies are shin- 
ing and translucent, sometimes altered in 
shape ; while the chromatin and finally the 
nuclei of the cell disappear (Fig. 27). 
The white infarctions of the spleen and 
kidneys, the areas of coagulation necrosis 
in tuberculosis, and the pellicle in croupous 
inflammation of the mucous membranes are 
the most common examples of this lesion. 

If, for example, in the spleen, one of 
the small arteries is plugged by an embolus, 
a corresponding portion of the spleen be- 
comes anaemic and appears as a white, 
wedge-shaped mass, sharply defined from 
the surrounding splenic tissue. If such a 
white infarction has existed but a short 
time there is hardly any difference between 
the appearance of its anatomical elements 
and those of the surrounding spleen, ex- 
cept that they are differently affected by staining-fluids. If the infarc- 
tion is older, the cells are small and shiny and their nuclei cannot be 
seen. 

In croupous inflammations of mucous membranes the epithelial cells 
become shiny, the nuclei disappear, and the shape of the cells is changed 
by the coagulation necrosis, so that a 
number of them together often look 
like a network of coagulated fibrin. 

Cheesy Degeneration (Caseation). — 
As commonly used this term embraces 
the changes in the tissues which we 
have just considered under the more 
appropriate name of coagulation ne- 
crosis. But it is also applied to that 
form of degeneration in which, under 
a variety of conditions, the dead tissue 
elements lose their normal structural 
features and become converted into an 
irregularly granular albuminous and 
fatty material CFig. 28) which some- 
times tends to disintegrate and soften, sometimes dries and becomes 
dense and firm, or may become infiltrated with salts of calcium. Thus 
cheesy degeneration may, and very often does, occur in tissu^es which 



W,^ 
t^^ j^-^ 



# 



$p'^ 



^ 






^ 
m 

K^ 






'^s^ 






Fig. 28— AN Arfv of Cheesy Degenirv- 
TioN (Caseation) in a Miliary Tubercle 
IN THE Lung. 



92 ATROPHY, DEGENERATION, PIGMENTATION, AND NECROSIS. 

are in the condition of coagulation necrosis ; but it also occurs in tissues 
which are not the seat of coagulation necrosis, but which, for a variety 
of reasons and in a variety of ways, have lost their vitality. 

The terms coagulation necrosis and cheesy degeneration, as com- 
monly used, in part actually cover the same degenerative conditions in 
the tissues. Both are indefinite, and will no doubt remain so until we 
gain a more precise knowledge of the conditions under which they occur. 

Fat Necrosis. — This is a degenerative process m.ost frequent near 
the pancreas, and especially associated with lesion of that organ. We 
refer for details to the special section, page 530. 

Fragments of dead tissues in the living body are in part disposed of 
by leucocytes or other mesoblastic cells which are attracted to them, and 
may cause their solution by a ferment substance which they set free, or 
by the incorporation of particles of the dead tissue into their bodies. 
Thus through chemotaxis and phagocytosis (see pages 111 and 115) 
considerable masses of necrotic tissue may be finally disposed of (see 
Fig. 44). 



CHAPTER III. 

HYPERTROPHY, HYPERPLASIA, METAPLASIA, 
REGENERATION. 

Hypertrophy and Hyperplasia. 

Under a variety of conditions, parts of the body or organs become 
larger than normal. The structural change to which this enlargement is 
due, may be a simple increase in size of the elementary structures of the 
part -cells, and other tissue elements. This is called simj^le hypertrophy. 
It is usually associated with some increased functional demand upon the 
cells ; as, for example, in the hypertrophy of the heart with lesions of 
the valves, or in the hypertrophy of one kidney, which in case of dimi- 
nution or suspension of function in the other assumes the work of both 
— compeimatory hypertrophy. ^ 

On the other hand, in many cases the increase in size of a part or 
organ is due not only, or not at all, to the increase in size of its elemen- 
tary structures, but to an increase in their number. This increase in 
number of the structural elements of a tissue or organ is called numer- 
ical hypertrophy, or hyperplasia.'^ 

Simple hypertrophy and hyx)erj)lasia are frequently associated. 

Metaplasia. 

The members of the connective-tissue group — fibrous tissue, mucous 
and fat tissue, cartilage, bone, etc. — are so closely related in nature and 
structure that not infrecxuently and under a variety of conditions one 
form of tissue assumes the characters of another. This change of one 
form of closely related tissue into another is called metajylasia. 

Thus, by a gradual change in the cells and stroma of fibrous tissue, 
this may be converted into bone, as mucous tissue may become fat tis- 
sue, and hyalin cartilage become fibrous. Metaplasia is a process in- 
volving active changes on the part of the living cells of the tissue, and 
should be clearly distinguished from certain degenerative processes, in 
the course of which one form of connective tissue may assume super- 
ficial resemblances to others of the grouj), as in calcareous and mucoid 
degeneration. 

AATiile metaplasia is most common among the members of the con- 
nective-tissue group, it sometimes occurs in other tissues. Thus, for 

^ For bibliography of compensator}' hypertrophy see reference to AscJwff, p. 106. 
'^ Consult for examples of hyperplasia and hypertrophy the following sections on 
Regeneration and Inflammation. ^ 



94 HYPERTfiOPHY, HYPERPLASIA, METAPLASIA, REGENERATION. 

example, the epithelium of the nose, bronchi, urinary passages, cervix 
uteri, and gall bladder, may under a variety of conditions assume the 
characters of squamous epithelium of the skin type/ 

It should be remembered that metaplasia occurs only within the limits 
of closely related tissues : when differentiation has advanced so that such 
distinct types of tissue have been formed as connective tissue, epithelium, 
muscle, nerve, these do not again merge through metaplasia. 

Regeneration. 

General Considerations, — It is during the earlier periods of life that 
the new formation of cells in the body is most active. From the fertil- 
ization of the ovum until the tissues and organs have assumed the varied 
forms and functions which the physiological division of labor among the 
cells imposes, cell proliferation and cell adaptation to a changing envi- 
ronment are constant and important features of individual development. 
After this time, under normal conditions, new cell formation is large- 
ly limited to the replacement of worn-out cells or to the restitution of 
such cells as may be sacrificed in the performance of their physiological 
functions. 

The studies of Bizzozero have slioM^uthat, notwitlistandiug the great diversity in 
the capacity for physiological regeneration among tissues, they may be conveniently 
grouped into three classes, as follows: First, tissues whose cells are capable of multipli- 
cation throughout the life of the individual or for a considerable period after maturity, 
and so lead to a continual regeneration. These are tissues whose cells are labile and 
evanescent. In this class are the parenchyma cells of those glands or structures which 
produce formed elements, such as the spleen, l3^mph-nodes, bone-marrow, ovary, testi- 
cle. Also the epithelium of the skin with its hair follicles and sebaceous glands, and of 
the mucous membranes of the respiratory, digestive, and genito-urinary organs. Sec- 
ond, tissues whose elements increase by division up to the time of birth, or sometimes 
for a short period thereafter, when evidence of physiological regeneration ceases. These 
are tissues with permanent cells. In this class are the parenchyma cells of those glands 
which secrete fluid material, such as the liver, kidney, pancreas, salivary glands, etc. 
Also members of the connective-tissue group, fibrous tissue, cartilage and bone, and the 
smooth muscle fibres. TMrd, striated muscle and nerve tissue. In these tissues, divi- 
sion by mitosis ceases at an early period and before the tissues have acquired their spe- 
cial characters. Here a physiological regeneration does not occur. 

This grouping of tissues in accordance with their capacity for physiological regen- 
eration, while liable to modification under further research, aifords a suggestive guide 
in our studies of regeneration under abnormal conditions. For beyond the regenerative 
capacity normally exercised by cells in response to the physiological wear and tear of 
life, they are frequently called upon to make good unusual losses, as the result of many 
forms of injury. 

Eegeneration of injured tissues, all new growths, as well as the 
hyperplasias above mentioned, are invariably brought about by prolifer- 
ation or other changes in living cells. Furthermore, just as the cells of 
the adult organism are the offspring of one original cell, the ovum, so 
are all the new cells which appear in the body under abnormal condi- 
tions derived from pre-existing cells by division. 

' For references to epithelial metaplasia see Menetrier in Bouchard's " Traite de Path, 
gen.," t. iii., pt. 2, p. 784. 



HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGENERATION. 95 

We shall now briefly suramarize the morphological changes which 
cells undergo in division and shall then indicate the degree of regener- 
ative capacity which various forms of tissues possess. 

MODES OF CELL DIVISION. 

The careful and minute study of cells during the act of division, 
which has been recently made, has revealed many most curious phe- 
nomena and has opened a new world of observation nearer to the elemen- 
tary expression of life than has seemed possible in earlier times. It will 
suffice for our purposes briefly to indicate some of the more striking feat- 
ures of the new cell lore. 

It is well to recall at the outset that recent studies of cells have shown 
that even in their simplest forms they are highly organized, and that 
their different parts have special functions to perform. Thus the nucleus 
presides over the constructive metabolism or assimilative process of the 
cell and furnishes the physical basis upon which the transmission of 
hereditary characters depends. The cytoplasm of the body, on the other 
hand, is concerned in those phases of metabolism which result in the 
liberation of energy in movements of various kinds and in the formation 
of new chemical substances. The centrosome also in certain cells, though 
not apparently in all, appears to play an important part in the changes 
incident to division. 

Two modes of cell division are commonly recognized. First, indirect 
division (mitosis, or karyokinesis) ; second, direct division (amitosis). 

Indirect (Mitotic) Cell Division. 

This is the most common mode of cell division and is especially char- 
acteristic of embryonic cells and those which are undergoing active de- 
velopment. While it presents great variations, its general features may 
be thus briefly summarized : 

Among the earlier changes which are to be seen in a cell about to 
divide by mitosis are a condensation and an increase in the staining capac- 
ity of the chromatin of the intranuclear network. This chromatin sub- 
stance gathers into a contorted thread or threads, called the spiremes 
(Fig. 29, 2), within the nucleus, whose membrane with the nucleolus 
gradually disappears so that the spireme lies free in the cytoplasm ; and 
at the same time with, or preceding, these changes in the nucleus, there 
may be a division of the centrosome when this is present, the segments 
resulting from this division passing to opposite parts of the cell, usually 
outside the limits of the nucleus. Around each of the new centrosomes, 
TN'hich stain deeply with hsematoxylin or other nuclear dyes, may be a clear 
zone of unstained material, or a series of fine radiating fibrils, or both ; 
the whole forming a structure called a polar body (Fig. 29, 2 and 3). 

Kow the threads of the spireme break across transversely, forming a 
series of more or less rod-like bodies called chromosomes, which form a 



96 HYPEftTROPHY, HYPERPLASIA, METAPLASIA, EEGENEKATION. 

somewhat flattened cluster or wreath between the polar bodies, lying in a 
plane at a right angle to a line passing between the latter. While this 
mass of chromosomes — sometimes called the monaster — has a stellar or 
wreath-like appearance when seen from the side, it is more band-like 
when viewed in profile (Fig. 29, 3 and 4). 

Between the polar bodies and across the monaster there may now be 
stretched a bridge or spindle of delicate fibrils resembling those about the 
centrosome in the polar bodies. 

This fibril-spindle, together with the polar bodies, is called the acmo- 





m 



X 



4% 

m9 



y 







6 

Fig. 39. 




'^'^S3-5S^ 



-Phases op Mitosis, 



1. Resting cell. 2. Spireme phase : the centrosome has divided, the polar body is seen ahove ; the nu- 
clear membrane has not yet disappeared. 3. Monaster phase : the polar bodies have arranged themselves 
on either side of the monaster here seen from the edge. 4. The monaster seen from the side. 5 and 6. 
Diaster phase : the chromosome clusters have separated and the achromatic figure is seen : in 6 the seg- 
mentation of the cell body has begun. 7. The completion of the nuclear division and segmentation of the 
cell body. 



malic figure in distinction from the structure formed from the chromatin 
which stains with nuclear dyes, and is called the chromatic figure. 

The whole complicated structure composed of both the chromatic and 
achromatic substance constitutes the mitotic figure. 

^ow each chromosome splits lengthwise into exactly equal parts. 
These i)arts separate into grouj)S which pass to the polar bodies at op- 
posite ends of the spindle. This is sometimes called the diaster phase of 
mitosis (Fig. 29, 5 and 6). 

Corresponding to the division of the chromosomes into equal parts, 
the cell body divides, each part containing one of the groups of daugh- 
ter chromosomes or diasters, together with one polar body and a part 
of the achromatic spindle (Fig. 29, 6). Now a new nucleus is formed 
about the daughter chromosomes which gradually assume the characters 
of the resting intranuclear network (Fig. 29, 7). The achromatic fibrils 
disappear from the new cell, while the centrosome m^ay also disappear or 
may take its place in the cytoplasm beside the new nucleus. 



HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGENERATION. 97 

There are countless variations and details in the minute processes of 
mitotic cell division and much interesting conjecture as to the meaning of 
the various changes in mitosis, which the scope of this work does not 
permit us to consider. But the facts already at hand are of extreme sig- 
nificance to the biologist and point toward large fields of research in 
pathology when the normal processes shall have been more clearly and 
exhaustively determined. 

Abnormal Phases of Mitosis are not infrequent. Thus the mitotic fig- 
ures may be asymmetrical, so that the distribution of chromatin sub- 
stance to the daughter cells may be unequal (Fig. 30). There may be 
multipolar mitosis, so that instead of two, several nuclei may form. Or, 
the new-formed chromosome 
masses may fail to share in the 
formation of the new nuclei. gj. ^ 

Such abnormal mitoses are '^ ^ 

frequent in certain tumors, and ^ 

they may be experimentally in- y^S^ 

duced by the application of vari- - 

ous chemical substances to living ^ .^„ ' 

^ FIG. -3U.— ABNORMAL PHASES OF MITOSIS. 

cells. Too little is known about ,^ ^,,^ ^^,,^ ^^^ ^^^^^,^ ,^ asymmetrical, and in the cell 

the conditions under which ab- to the left tnpoiar. 

normal mitoses occur, and too 
%^little about the nature of the impulse to cell division in general, to 
justify to-day far-reaching conclusions as to the significance of these 
interesting abnormalities in the life of the cell. 

The Significance of Mitosis. — The term mitosis or Ticiryomitosis is api^lied 
to this indirect mode of cell division, on account of the involvement of 
the nuclear threads. It is also sometimes designated as JcaryoJcinesis, from 
the form changes which these threads undergo. Aside from its intrinsic 
biological interest, a knowledge of mitosis in proliferating -cells is of im- 
portance in pathology, because the recognition of mitotic figures often 
enables us to decide with certainty what particular cells or cell groups 
are involved in the formation of new tissue. The most significant feat- 
ure, however, of the whole process of mitosis, with all its intricate 
variations, appears to be that the chromosomes, during their separation 
into two or more clusters to form the basis of new cells, undergo an exact 
longitudinal division. So that, under normal conditions, no matter how 
unequal the division of the cytoplasm may be, all of the new nuclei share 
alike in the chromatin substance of the parent nucleus. This fact ap- 
pears to be of extreme importance in the recognition of a physical basis 
of inheritance. ' 

Direct (Amitotic) Cell Division. 

In this, which although relatively rare appears to be the most simple 
mode of cell division, without those preliminary changes in the nucleus 

^ See reference to summary by AVilson, pp. 272 and 273. 



mmm 



98 HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGENERATION. 

which are seen iu mitotic cell division, the nucleus with its membrane 
becomes constricted and finally divides into two or more parts which be- 
come new nuclei. At the same time or following this simple nuclear 
division the cell body divides, and thus two or more cells may form iu 
the place of one. Sometimes the nuclear division is not followed by a 
division of the cell body, and thus multinuclear cells, or ''giant cells ^^ 
may be formed. 

The signifiance of the difference between the amitotic and the mitotic 
cell division is that, while in the former there is an exactly even division 
of chromatin to the daughter nuclei, the division in the latter is of the 
nuclear mass as a whole. 

Amitotic, as well as mitotic, division occurs in leucocytes, in some 
forms of epithelium, and in pathological new formations. While the na- 
ture of the process is little understood, there appears to be much reason 
for the belief that, in general, amitotic division is "characteristic of highly 
specialized or degenerating cells in which dcA^elopment is approaching its 
end.^'^ 

GENERAL CHARACTERS AND LIMITATIONS OF CELL 
REGENERATION. 

It should be borne in mind, in studying the regeneration of various 
kinds of cells and tissues, that the acquirement by certain cells of special 
functional powers as the result of the physiological division of labor has 
involved the impairment of some of their more primitive general capac- 
ities, among these that of reproduction. Thus it is that we find in the 
ganglion cells an almost total lack of reproductive capacity ; while in 
many of the gland cells this is slight, in others considerable. In some of 
the less highly differentiated cells of the body, on the other hand, as in 
certain forms of epithelium, in blood cells, and, in the cells of the con- 
nective tissue, this primitive capacity of protoplasm to form new simi- 
lar cells by division is maintained, and may be evoked by the changed 
conditions which injury or loss involves. 

Although the occurrence of mitosis is the mark by which we espe- 
cially recognize the regenerative process in cells, it should be remembered 
that mitosis or some of its phases may occur in cells, without being fol- 
lowed by those further changes which lead to new cells or new tissues.^ 

We may also often recognize new-formed cells and tissues by differ- 
ences in the shape and character of the cells and the arrangement of the 
tissue elements, these often approaching the embryonic type in form as 
well as in character of development. Furthermore, the atypical arrange- 
ment often seen in new -formed cells, both in regard to each other and in 

' For a comprehensive summary of facts and theories concerning the cell, both in 
higher and lower forms of life, consult Wilson 's masterly work, " The Cell in Develop- 
ment and Inheritance," 1900. 

■^ One is often disappointed in seeking for mitotic figures to find so few of them even 
in rapidly growing tissues. This is due to the fact that cell division even when active 
is not continuous, and periods of rest may follow the act of division. See Thoma's 
"Text-book of General Pathology," English Tr., vol. i., p. 481. 



HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGENERATION. 99 

their association with older tissues, may aid in the identification of the 
formative i)rocess. 

Individual cells may, even after having undergone marked vStructural 
changes — as, for example, in albuminous degeneration — or after a 
certain degree of physical injury, be restored to a normal condition. 

After destructive injury or loss a full and complete replacement of 
cells and tissues can occur only as the result of a proliferation of cells of 
the same type as those to be restored. Thus a regeneration of epithe- 
lium occurs by proliferation and growth of epithelial cells alone ; regen- 
eration of muscle by muscle cells, etc. In fact, however, in the higher 
types of tissue, after considerable injuries with loss of substance or after 
destructi\'e pathological processes, complete regeneration is not common. 
This, as we have seen, is because the highly specialized cells of the body 
are limited in their capacity for reproduction closely to the domain of 
physiological regeneration. What we ordinarily call healing in extensive 
wounds of the more highly specialized tissues is usually a j)rovisional 
makeshift repair by means of new-formed connective tissue. 

We have seen that the regenerative capacity in the cells of the human 
body is most marked in the less highly differentiated tyj)es of cells, and 
that it is above all the connective tissue, blood-vessels, and epithelium 
which most frequently and most completely undergo regeneration. 
These are relatively lowly organized tissues and serve for the mainte- 
nance or protection of more highly specialized tissues, and with them 
regeneration may be comi3lete with full restoration of function. But 
although the more highly organized tissues in man do not undergo after 
injury any considerable regeneration, they are, when uninjured, capable, 
under the stimulus of increased functional exercise, of compensatory 
hypertrophy, so that the loss to the organism of similar tissue may be 
made good. A common example of this is the structural hypertrophy 
and increased performance of one kidney after the removal of the other. 

The capacity to regenerate lost or injured parts exists to a certain 
extent in all animals but is most marked among the lower forms. Thus 
if an amoeba be cut in two so as to leave one part with the intact nucleus, 
this part lives and the one -celled organism is completely restored. The 
fresh-water hydra, composed of many cells, may reproduce a large por- 
tion of the organism from a small severed fragment. The common earth- 
worm can reproduce a severed head or tail. Crabs reproduce a whole leg 
if the severance takes place at a particular joint. Salamanders, snails, 
etc., can reproduce leg and tail. Is is further noteworthy in this con- 
nection that the larvae of many lower forms, such as reptiles and insects, 
have a much greater capacity for the reproduction of lost parts than the 
same species have when in the adult condition. 

REGENERATION OF SPECIAL TISSUES. 

Regeneration of the Nerve Tissue. — In the nervous system we find no 
evidence that the ganglion cells are capable of reproduction. Some phases 
of mitosis are occasionally found in them, although they do not appear 

LofC. 



100 HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGENERATION". 

to lead to proliferation. But if tlie essential i^arts of the ganglion cells, 
including the nuclei, be intact, a restoration may occur of their central 
as well as their peripheral branches. The iibrous and the neuroglia tis- 
sue of the central nervous system, on the other hand, may increase, and in 
this way, even with considerable loss of substance, injuries to the brain 
and cord may undergo a sort of ijatchwork repair. 

In the peripheral nerves a considerable regeneration of fibres may 
take place after injury, when the corresponding ganglion cells are intact. 
This restoration may be effected in part by fibrous tissue which bridges 
the damaged region and affords guides or channels along which the axis 
cylinders may grow out from the uninjured central segments, finding 
their way to their endings, as in embryonic develoiDment they stretch 
into the tissues far from the ganglion cells in which they originate. The 
restitution is possible here because the centre of nutrition and at least a 
limited reparative control in the ganglion cell are intact. 

Further details as to degenerations and regenerations of nerves and 
nerve tracts may be found in the chapter devoted to The I^ervous 
System. 

Regeneration of Muscle Tissue. — Regeneration of smooth-muscle tissue 
after injury is slight. Mitosis may occur in the cells and iDreliminary 
phases of division of the body have been described, but it is doubtful 
whether, except possibly to a very slight extent, new cells are formed. 
Such healing as occurs after wounds and other injuries is largely effected 
by new-formed fibrous tissue. 

A partial regeneration of striated muscle occurs after various form of 
damage and losses of substance. There may be division by mitosis in 
the sarcolemma nuclei (Fig. 31) associated with the accumulation near 
them of granular protoplasm, which becomes striated, either in situ or 
as independent cells. At the injured end of the muscle fibre a similar 
process may occur, so that these damaged fibres may be in part restored. 



~ ''r<ii^-- r^ ^^ 



(^ 



Fig. 3L— Regeneration op Striated Muscle after Injury. 

The nuclei of the sarcolemma have proliferated and are surrounded by a small amount of non-striated pro- 
toplasm. 

If as the result of the injury some of the nucleated protoplasm escapes 
from the sarcolemma, a similar development of striated cells and cell 
masses may occur. 

It is especially in certain forms of degeneration of the contractile 
substance, after typhoid fever for example, in which the nuclei, the sar- 
colemma, and the general framework of the tissue are uninjured, that 
regeneration of striated -muscle fibres is most complete. After injuries 
with considerable destruction of the muscle tissue, regeneration is apt to 



HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGEK^ERATION. 101 

be irregular and incomplete. A^Tiile there is often much nuclear divi- 
sion and often the formation of large numbers of more or less striated 
and variously shaped cells, these are apt not to develop into useful 
muscle fibres and may disappear by degeneration and absorption or by 
pressure atroi^hy. Here, as elsewhere in highly organized tissues, such 
restitution as is possible after considerable injury is achieved by fibrous 
tissue. 

It is interesting to note that such regeneration as does occur in 
striated muscle is not initiated by the highly differentiated contractile 
substance, but by the nuclei and small residual amount of undifferen- 
tiated protoplasm, and that such more or less definitely striated cells as 
are formed, are in many respects similar to certain forms of developing 
muscle cells in the embryo. 

Although mitosis and nuclear division have been seen in the muscle 
fibres of the heart after injury, there is no evidence that new muscle can 
be formed. Eepair, which is not infrequent, is secured by fibrous tissue. 

Regeneration of Epithelium. — Owing to continuous shedding or to 
functional destruction of epithelium of the skin and mucous membranes 
and certain of their adnexa, physiological regeneration by mitosis is 
common. 



r^^^d-IM^. 






-£ y'^i^'^, 



;^vy-& 





















Fig. 33.— Regexeration op Epithelium. 



From a wound of the tongue. At the left Is normal epithelium ; at the right the thin pellicle of new formed 
cells is extending over the surface of the wound. 

After injuries also regeneration of epithelium in these situations oc- 
curs by mitosis and may be extensive and complete. The new epithelium 
always forms from the old, and, when surface losses are to be made good, 
extends inward from the edges across the injured area after a suitable 
substratum has been formed by fibrous tissue and blood-vessels (Fig. 32). 
The new epithelium is at first atyi^ical in form and arrangement owing 
to the necessity for a gradual adaptation to the sustaining and associated 
tissues. Thus the epithelium, which at first presses forward over a heal- 
ing wound of the skin, may be in the form of a single layer or a thin 
smooth pellicle without the usual variations in size and shaj^e by which 
it is later characterized when the papillae of the new cutis are formed, 
and the new cells have adjusted themselves to these and to each other.' 

In stratified epithelium it is the deeper layers from which the new 

' For a study of the regeneration of mucous membranes see Cornil and Carnot, 
Arch, de Med. Exp., tome xi., p. 413, 1899. 



102 HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGENERATION. 

cells chiefly arise. A^Tiile amitotic division has been observed in the 
restitution of surface epithelium, this occurs in the more superficial cells 
and is believed not to be concerned in the regenerative process. 

Eegeneration of gland epithelium after injury is of frequent occur- 
rence, though this capacity varies considerably in different glands. In 
many cases it appears to be by a proliferation of the epithelium lining 
the smaller excretory ducts that the restitution is accomplished, rather 
than by the more highly differentiated secreting cells. This is of espe- 
cial interest because it affords an excellent example of the rehearsing under 
abnormal conditions and for reparative ends of a developmental phase 
of cell life. 

In the liver very extensive new formation of liver cells may occur 
after exiDcrimental removal of a portion of the organ. In the thyroid 
gland also new gland tissue may be formed after injury. In the kid- 
ney the regenerative capacity of the epithelium appears to be less 
marked, though proliferation of the epithelium of the collecting tubes 
may take place. But in all these cases it is often difficult to determine 
how much of the increase in parenchyma, which undoubtedly may occur, 
is due to a formation of new gland tissue and how much to a compensa- 
tory hypertrophy of the old. 

While, therefore, it is true that after injuries to the glands a consider- 
able regeneration of epithelium may occur, when the loss of substance 
is extensive it is usually rather by a fibrous-tissue repair or by a com- 
pensatory hypertrophy or hyperplasia in the uninjured portions of the 
organ than by the new formation of true gland tissue that restitution 
occurs. 

Regeneration of Connective Tissue, — We have seen again and again in 
reviewing pathological regeneration that, in local restoration after in- 
jury, fibrous tissue plays an important i)art, either by itself or in asso- 
ciation with various forms of parenchyma. New fibrous tissue may be 
formed in the adult to replace tissue which has been destroyed. It re- 
sults from many kinds of prolonged chemical and mechanical irritants. 
Thus atrophy of the parenchyma may be followed by interstitial fibrous- 
tissue growth, or new fibrous tissue may develop under the influence of 
bacterial and other toxic substances, and it frequently forms dense cap- 
sules about the seat of old lesions or around foreign bodies. 

Many forms of compensatory fibrous- tissue development will be de- 
scribed in the second section of this book, such as thickening of the 
walls of blood-vessels, inflammatory adhesions, replacement hyperplasia, 
etc. 

We have now to consider briefly the changes involved in the new 
formation of this fibrous tissue. Here, as in all other tissues of the hodj, 
it is the cells alone which take the initiative, the formation of intercel- 
lular substance being always secondary to the formation of the cells and 
always occurring under their influence. 

New connective -tissue cells may be formed by mitosis, either from 
older connective-tissue cells, or, as now seems certain, from the endothe- 



HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGENERATION. 103 

linm of the blood-vessels and possibly from the so-called '^ plasma cells. ^' ' 
111 either case the cell about to divide shows an increase in the size 
of the body, which becomes more granular; the nucleus divides by 
mitosis, segmentation of the cytoplasm following. This process may be 
repeated so that many cells are derived from one, separated at first by 
a small amount of homogeneous intercellular substance. These cells, 
at first more or less spheroidal in form, may become larger, and poly- 
hedral or elongated. Little by little, fine fibrils appear between the 
cells, sometimes apparently as extensions of their cytoplasm, sometimes 
along their sides in the homogeneous material in which they lie. Such 
new connective-tissue cells concerned in the formation of fibrillar stroma 
are caWed fbroMasts (Fig. 33). As the fibrous stroma increases in amount 









f 



^^ 




Fig. 33.— Regeneration of Connective Tissue. 

Showing fibroblasts with a few new-formed Intercellular fibrils between them. The vessels have 
thin walls, and a few leucocytes have passed through them into the tissue. A mitotic figure is shown in the 
left lower portion. 

the cells, at first relatively abundant, become elongated and flattened, 
until as the new tissue approaches maturity the more or less dense 
fibrillar stroma preponderates, pressing the cells between its bundles 

' Plasma Cells. — It is believed by many that the so-called plasma cells are fre- 
quently and largel}^ concerned in the formation of new fibrous tissue. Plasma cells 
are rounded or polyhedral or elongated, depending upon their situation, and vary in 
size from that of a leucocyte to many times this size. The rounded or oval nucleus is 
usuall}^ excentric and commonly shows several irregular groupings of chromatin masses 
just beneath the membrane. The body of the plasma cell is especially characterized 
by the staining of its protoplasm by basic anilin dyes — the polychrome methylene blue 
of Unna, for example. The staining is commonly less intense near the nucleus and is 
otherwise freciuently uneven. 

Such cells occur normally in the bone marrow, spleen, h^mph nodes, and gastro- 
intestinal mucosa of man, and may be found under various pathological conditions, 
especially in hyperplasia and the new formation of fibrous tissue. It is believed by 
many observers that plasma cells are direct derivatives of the small mononuclear 
lymphocytes, and that when these gather in the tissue by emigration the}^ may either 
undergo degeneration and destruction, or, on the other hand, that they may "become 
connective-tissue cells and share as fibroblasts in the formation of fibrillar stroma. The 
origin and significance of " plasma cells " is not yet altogether clear, and we must refer 
to larger works for further data. See "' Critical Summary of Recent Literature," by 
Williams, American Journal of the Medical Sciences, vol. cxix., p. 702, 1900. 



104 HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGENERATION. 

or layers into variously shaped plaques, often fusiform or linear in 
profile. 

In the formation of fibrillar connective tissue from endothelium the 
endothelial cells of thin-walled blood-vessels increase in size, stretch 
slender bud-like extensions into the adjacent tissue, where, after mitotic 
division, they assume a role altogether identical with that of the ordinary 
connective -tissue cell. 

The formation of new connective -tissue cells may be large or it may 
be limited to the production of a single pair of cells ; the stroma may be 
scanty or abundant, loose or dense ; the process is essentially the same, 
namely, the division of cells by mitosis, and the formation by them, or 
under their influence, of more or less fibrillar stroma. This process, it 
will be seen, is practically identical with the formation of fibrous tissue 
in the embryo. 

But here, as elsewhere, the character and extent of new tissue pro- 
duction are largely influenced by the environment, and particularly by 
the nutritive supply, so that the formation of ncAv connective tissue in 
any considerable amount is closely linked to the development of blood- 
vessels. 

The Formation of Blood-Vessels. — The formation of blood-vessels in 
post-embryonic life is believed always to start in a budding or sprouting 




Fig. 34.— Developing Blood-vessels in New-formed Tissue. 



of the endothelial cells of pre-existing capillaries. The sprouts, directed 
outward from the endothelia of the capillaries, consist at first of slender, 
conical, or filiform projections of cytoplasmic substance (Fig. 34). K^ow 
the cytoplasm of the cell from which the sprout springs may increase in 
amount and its nuclei divide by mitosis, so that the base of the sprout 
may consist of a multinuclear mass of cytoplasm or of a cluster of new- 
formed cells. The sprouts may extend for a long distance into the sur- 
rounding region, whether this be already organized tissue in which the 
vessels are increasing in number or unorganized lifeless material like 
blood clot, which is to be replaced by new living structures. If a similar 
process be in progress in neighboring vessels, the sprouts may unite at 



HYPEETEOPHY, HYPEEPLASIA, METAPLASIA, EEGEKEEATION. 105 

their extremities, forming a slender solid protoplasmic bridge from ves- 
sel to vessel. The sprouts now become thickened and gradually chan- 
nelled out at the base by pressure of the blood in the vessel from which 
they spring. The blood enters these lengthening channels, forcing its 
way along them, forming a lumen as it goes. Simultaneously with this 
advance of the lumen, new nuclei are formed by division of the old along 
the sides of the vessel, and the new structure gradually assumes a dis- 
tinctly cellular and vascular character. At length the channel is com- 
plete ; the new vessels have well-defined endothelial walls and connective- 
tissue cells from without, or new connective -tissue cells which have been 
formed about the nuclei of the protoplasmic sprout, range themselves 
outside along the walls. So the new vessel takes its place in the vascular 
system of the part. Thus, in a short time, many new blood-vessels may 
form, furnishing ^lutritive centres about which the organization of tissue 
proceeds. 

In the new formation of arteries it is believed that the smooth-muscle 
tissue is formed by a growth along the developing vessel from a pre-ex- 
isting artery. 

Regeneration of Cartilage and Bone. — Xew cartilage may form by the 
proliferation, either of connective -tissue or, to a slight extent, of cartilage 
cells and the formation about the new cells of the characteristic basement 
substance. 

The new formation of hone under pathological conditions takes place 
by the development, first, of fibrillar connective tissue or of hyaline 
cartilage. These tissues, especially through the influence of periosteal 
cells, undergo by metaplasia a gradual conversion into characteristic 
bone tissue. This mode of bone formation is essentially similar to that 
in embryonic development. See Fig. 393, p. 662. 

Regeneration of Blood. — The formation of leucocytes ai^pears to occur 
chiefly in the masses of lymphoid tissue which are so widely scattered 
in the body in the lymph nodes, in the spleen, and in the bone marrow. 
Both mitotic and amitotic cell division are to be observed ii^ the new 
formation of leucocytes, but the exact relationship between the new cells 
produced in these two ways, and their respective destinies, is not yet 
very clear. Eegeneration of red blood cells seems to occur in the bone 
marrow through mitotic division of nucleated forms. The latter may, 
under iDathological conditions, appear in the vessels in varying numbers 
(see Part III., Chapter I.). 

THE IMPULSE TO CELL REGENERATION. 

While we can thus summarize the ditf ering capacities of the body cells 
for regeneration, while we know many of the general conditions under 
which the impulse to cell proliferation and growth is manifested, while, 
further, we have learned something of the delicate mechanism through 
which division is controlled and effected, at the end we must acknowl- 
edge that we do not know whv cells divide. AVe mav sav that it is due 



106 HYPERTROPHY, HYPERPLASIA, METAPLASIA, REGENERATION. 

to a chemical or a mechanical stimulus, and it certainly may be asso- 
ciated Avith both, or that increased nutrition favors while innutrition 
retards cell multiplication; we may cite direct or remote injury, or talk 
of the inhibition of organic control, disturbed tissue equilibrium, dimin- 
ished pressure, etc. , but when all is said we are forced to recur to some 
unknown factor in the inherited constitution of the cell which determines 
the measure and character of its response to the most varied influences. ' 

1 Consult in this connection, for bibliograpli}' on the formative stimulus, references 
on the Origin of Tumors, p. 272. 

See also, for summary of a new phase of research and interpretation in the nature of 
the "formative stimulus" involved in artiticially induced cell division and artificial 
parthenogenesis, Mattheim, Journal of the Boston Society of Medical Sciences, vol. v. , 
p. 13, 1900, Bibl., and for a review of recent advances in the knowledge of the cell, 
Wilson, "Some Aspects of Biological Research." The International Montlll3^ July, 
1900. For general bibliography of regeneration, compensatory hypertrophy, etc., see 
Aschoff, Lubarsch and Ostertag's Ergebnisse, Jahrg. v, for 1898, p. 22. 



CHAPTER IV. 

INFLAMMATION. 

General Considerations. 

The conception of inflammation was originally a clinical one in which 
the process was marked by symptoms — redness, heat, swelling, pain, and 
impaired function. This conception was gradually enlarged to embrace 
the new formation of tissue which inight be associated with or follow 
these symptoms, or which might be independent of them. After the 
knowledge of the importance of the cell became general it was upon the 
formation and accumulation of cells and other substances that attention 
was especially fixed. Finally, the processes and structural alterations 
embraced in the conception of inflammation became so varied and com- 
plex that a definition or even a characterization seemed not only difficult, 
but wellnigh impossible. 

It is only within the past decade or two that the processes and lesions 
involved in inflammation have been seriously considered in the light of 
comparative pathology and as biological problems divorced for purposes 
of research from the dominance of traditional clinical conceptions. In 
view of our increased knowledge of the structure of cells, and of the im- 
pulses immediate and hereditary which determine their performances, it 
seems possible now to resolve the complex processes and lesions embraced 
in the general notions of inflammation into more simj)le factors, and to 
arrive, if not at an exact definition, at least at a reasonable conception of 
the relationshij) of its phenomena to each other, to those of normal physi- 
ology, and to other phases of disease. 

With this end in view it seems wise at first to rehearse as simply and 
briefly as is practicable some of the more typical of the phenomena and 
lesions which are commonly groui^ed under the term inflammation. 

While the death of tissue from trauma and degenerative alterations 
in the tissues in the presence of various form of poisons are often impor- 
tant factors in the inflammatory processes, we shall not consider them 
separately here, because they are incidental rather than inherent and 
have already been treated in the section on degenerations and necrosis. 
But it should be noted that various phases of albuminous degeneration, 
local or general, which are induced by the poisons of the pathogenic 
bacteria, are very often associated with inflammation, and not infrequently 
modify, or may even determine, its occurrence. 

A comi^rehensive survey of the conditions under which inflammation 
most frequently takes place shows at once that it is almost always asso- 



108 INFLAMMATION. 

ciated with some form of injury. This may be direct trauma, or exces- 
sive heat or cold. It may be poisons of various kinds — from the cruder 
inorganic poisons inducing immediate and gross tissue destruction to the 
subtle toxic substances which result from the metabolism of micro-organ- 
isms or from the aberrant metabolism or degeneration of the body cells 
themselves. 

Let us now look at some of the ways in which the living body re- 
sponds to injury, and first at an injury which is very slight and simple. 

Types of the Inflammatory Reaction of the Body to Injury. 

Injury to Non-Vascular Tissue. — If a small clean cut be made in liv- 
ing fibrillar connective tissue, not involving blood-vessels and affecting 
only the cells and fibres in the vicinity of the incision, and if the sides 
of the wound be immediately placed and held together, the resulting 
changes which lead to the complete restitution of the part are compar- 
atively simple. A small quantity of fluid which oozes from the tissue 
spaces sticks the sides of the cut together. Such connective -tissue cells 
as have been seriously injured, especially if the nuclei have suffered, die 
and disintegrate. But cells whose nuclei have remained intact, whether 
directly upon the incision or in its immediate vicinity, become larger and 
more granular, may divide by mitosis, extend their bodies or processes 
across the plane of incision, bridging this at intervals with living proto- 
plasm. Under the influence of these cells, new intercellular fibres are 
formed, which in a short time bind the sides of the wound firmly together. 
Thus with but the slightest amount of tissue destruction, and with no in- 
volvement of the blood-vessels, a simple mechanical injury may be made 
good. This form of reaction to injury of living tissue is known to the 
surgeons as healing by first intention. The mode of healing does not essen- 
tially differ if there be a slight injury to the blood-vessels. 

Injury to Vascular Tissue. — Let us now look at the effect on a vascular 
tissue of an injury not immediately destructive. For this purpose the 
mesentery or the bladder of a curarized frog, drawn out upon a suitable 
plate upon the stage of the microscope and kept moist by irrigation with 
three-fourths-per-cent salt solution, affords a succession of most instruc- 
tive pictures. The mechanical disturbance of the organs exposed, desic- 
cation, and a variety of other phj^sical and chemical vicissitudes to 
which they are subjected are sufficiently damaging to incite a complex 
train of responses on the part of the living tissues. 

In studying the circulation of the blood in small vessels under the 
microscope it should be remembered that, while the walls of these ves- 
sels are made up of living tissue and are capable of responses by move- 
ment or by structural change to external agencies, whether api)lied direct- 
ly or through the nerves, they are also elastic pii^es through which fluid 
flows, and that both pipes and fluid are subject to the laws of mechanics. 
These mechanical laws are often modified in expression, it is true, by the 
subtle energies which living tissues wield, but, as Thoma more than any 



INFLAMMATION. 109 

other has shown, they are not to be ignored by the serious student of the 
living body, either in health or disease. 

In the bladder or mesentery of the frog the arteries and veins with 
their connecting system of capillaries are clearly seen. When the cur- 
rent is rapid the cells of the blood in the arteries and veins are gathered 
into a red axial mass in which the separate cells may not be distinguish- 
able, owing to their crowding and the rapid flow. Outside of this, against 
the walls, is a clear marginal zone in which a leucocyte is occasionally 
visible. If for any reason the rate of flow be considerably diminished, 
the leucocytes, which are specifically lighter than the red cells, gather in 
the marginal zone. If the current become very slow or be arrested, the 
marginal zone disappears and the red and white cells intermingle. ' 

Soon after the exposure of the bladder or mesentery the arteries, 
veins, and capillaries dilate, and the blood, encountering less resistance 
from the walls, flows more rapidly through them. This increased rapid- 
ity of the blood current does not, however, last long, although the vessel 
still remains dilated. After a variable period, owing, it is believed, to 
changes in the endothelia of the vessels, the blood meets with so much 
resistance that it flows more slowly than under normal conditions. Tem- 
porary or even permanent stasis may occur in some of the vessels, but 
this is not a constant nor a characteristic occurrence. White blood cells 
— leucocytes — now begin to accumulate along the inner walls of the veins 
and to become fixed there, so that after a time the whole inner surface of 
the veins may be more or less thickly sprinkled, and even closely crowded, 
with adherent leucocytes. These may either lie firmly against the endo- 
thelium or be dragged slowly along by the current of blood sweeping 
past them. Some are dragged by the blood current into pyriform 
shapes, showing that they are adherent at a small point only, and thus 
they may be detached from the wall and rejoin the circulating blood. 
They may by amoeboid movement crawl slowly along the interior of the 
wall, even against the current. In the capillaries, also, a similar com- 
portment of the leucocytes may be seen. 

After a time, which varies considerably — in the bladder sometimes 
within an hour after its exposure ; in the mesentery usually later — some 
of the leucocytes commence to make their way slowly through the walls 
of the A^eins and capillaries. At first a little shining knob appears on 
the outside of the wall opposite to the cell which is sticking within, and 
this outer portion grows larger as the part still within grows smaller, 
until at length the entire cell is outside of the vessel. The cell now may 
immediately detach itself and wander off in the tissue spaces, or it may 
remain for some time attached to the outside of the wall (Fig. 35). This 
passage of the leucocytes through the walls of the capillaries and veins — 
it does not occur in the arteries — is called emigration. The emigrating 

^ This distribution of the blood is almost, if not wholly mechanical, and may be 
simulated in glass tubes with a fluid in which lifeless particles of different specific 
gravities are suspended. The particles of the lesser specific gravity assume, when the 
flow is established, the peripheral portion of the stream. 



110 INFLAMMATION. 

cells are largely the polynuclear leucocytes, but mononuclear forms and 
eosinophiles may also pass out of the vessels. 

The cells pass between the endothelia through the cement substance, 
which apparently is in some way changed in the inflammatory process. 



if- 



!::.-■ 4 



^f 



\ 






Fig. 35.— Emigration of Leucocytes from the Blood-vessels of the Mesentery of the Frog. 

Some of the leucocytes are clinging to the interior of the vessels ; some are passing through the walls ; some 
are wandering away through the tissue spaces. There has been diapedesis of a few red blood cells. 

They may pass through very rapidly, but usually their i)rogress is slow 
and often interrupted, so that cells may be seen motionless for a long 




Fig. 36.— Exudatite Inflammation in the Wall of the Appendix Vermiformis. 

Showing extravasated leucocytes in the vicinity of the blood-vessels with oedema of the surrounding con- 
nective tissue. 

time in various stages of progress through the walls. A half minute, or 
even less, may suffice for their passage, or they may be hours about it. 
Thus, after a variable time, if the conditions have been favorable, the 



INFLAMMATION. Ill 

tissues immediately around the capillaries and veins, and even those 
somewhat remote from them, may be more or less densely crowded with 
leucocytes, some motionless and in the spheroidal form, others moving 
about through the tissue spaces (Fig. 36). Leucocytes may pass out of 
the tissues on to free surfaces of the inflamed part, or they may wander 
into the lynij)h-^'essels and so re-enter the circulation. 

It is probable that the emigration of the leucocytes is due in part to 
a sort of filtration process with which the pressure of the blood within 
the vessels is concerned, and also to capillary attraction at the point of 
emergence. But the inherent contractility of the cells themselves forms, 
doubtless, a very important factor. That in most cases chemotaxis plays 
a significant part in directing the course of the leucocytes seems to be 
well established, and it is largely to this that the gathering of leucocytes 
is due in the vicinity of the deleterious agents which incite inflammation. 
In regard to chemotaxis it should be said in brief that the direction of 
locomotion in protoplasm may be determined by chemical substances in 
the vicinity. This is the case not only in the lower forms of life, as in 
certain bacteria and i^rotozoa, but also in such cells of higher organism 
as have retained a certain independence of locomotion, for example, in 
the leucocytes and certain cells of the connective tissue. To this form of 
response to external agencies the name chemotaxis has been applied. In 
some cases the effect of chemical agents in the environment is not to at- 
tract, but to repel i3rotox)lasm. This has been called negative chemotaxis. 
Chemotaxis and certain allied responses to outside influences have been 
found to play an important role in health as well as in some forms of 
disease, and have been the subject of much careful study.' 

If we return now to our observation of the living mesentery it will be 
found that while emigration of leucocytes is going on the red blood cells, 
although for the most part carried along as usual in the current of the 
veins and through the capillaries, still often find their way in small, and 
sometimes in very large, numbers into the surrounding tissues. They are, 
it is believed, carried passively through the cement substance between 
the endothelia by minute streams of fluid which under these conditions 
are flowing in abnormal quantities through the walls. This extravasa- 
tion of the red blood cells is called diapedesis. It appears to follow the 
emigration of the leucocytes, which seems in some fashion to prepare the 
way for the more mechanical exit of the red cells. 

By this time it will be usually found that the tissue around the ves- 
sels is somewhat swollen and more succulent than normal, and fluid may 
be poured out on the free surface. The fluid which thus gathers is called 
senim. It is similar to the simple non-inflammatory transudates, except 
that it is richer in proteids and is mixed with cells. This serum has 
passed out of the blood-vessels along with the blood cells, and, as its 
composition differs somewhat from that of blood plasma, it is evident 

' For a fuller consideration of chemotaxis, with bibliography, consult DciTenport, 
"Experimental Morphology," Part I., p. 32, et seq. For the forms of leucocytes which 
emigrate under various conditions see Adler, A. Jacobi's Festschrift, 1900, p^BOO. 



112 



INFLAMMATION. 




Fig 



that it has undergone a change as it passed. The way in which this 
alteration in the composition of the bkiod x>l<isiii*^ occnrs as it passes 
throngh the walls of the vessels and becomes the sernm of exndation, we 

do not nnderstand. Bnt it is probably due 
to metabolic xn-ocesses in the endothelial 
cells by which what has been called a ^^se- 
lective filtration " is secured. 

The fluid exudate contains tibrinogenous 
substance, and from this, when the condi- 
tions are favorable, fihrin may be formed 
(Fig. 37) by a change similar to that which 
occurs in tlje coagulation of the blood. The 
leucocytes which wander into the tissue 
spaces outside the vessels may encounter 
conditions inimical to life, from innutrition or from the presence of dele- 
terious substances, and thus these and other cells furnish as they die and 
disintegrate the fibrin ferment essential to coagulation. Clusters of 
fibrin fibrils may thus often be seen surrounding dead and disintegrat- 
ing cells (see Fig. 38).^ 

If at this time the exjDOsed bladder or mesentery of the frog be re- 
stored to the abdominal cavity and the animal placed under favorable 
conditions, the reaction of the vessels and cells to the unusual environ- 
ment may, if the injury have not been too severe, gradually subside. 
The circulation is then re-established, the serum is absorbed, the leuco- 
cytes which h9,ve not come out upon the surface or died in the tissue 



37.— FiBRix IN Inflammatory 
Exudate. 




FiCx. 



-Fibrin Forming Around Dead Cells in the interstices of Tissue. 



spaces may re-enter the lymphatics. Fibrin, if this have been formed, 
and red blood cells which have escaped from the circulation are dis- 
posed of by simple decomposition, or under the influence of ferments 

1 For a discussion of the relationship of fibrin formation to cells which may furnish 
a substance inducing coagulation see Hcmser, Virch. Arch., Bd. cliv., p. 335, 1898; also 
Arnold, Cbl. f. Path., Bd. x., p. 313, 1899. 



INFLAMMATION-. 



113 



which leucocytes furnish (see p. 116), or may be carried off by the wan- 
dering leucocytes; or, as is not infrequently the case, the decomposed 
blood iDigment may remain for some time, in situ, as the only mark of 

an earlier active inflammatory 






'^'^'""f^^fe 



«^ !fc- 












it '" 



:^^^. 



^ , 

« 



V 






-^\V#^' 






Fig. 39.— Bacterial Embolus m the Liver. 

The bacteria have grown in a mass within the small 
blood-vessel. The liver cells in the vicinity appear un- 
changed. 



process. 

Thus in the living animal ' 
we can' learn by direct obser- 
vation the way in which serum, 
fibrin, and red and white blood 
cells get into the tissues and 
upon free surfaces in certain 
forms of injury involving the 
blood-vessels. These materials 
gathering in or upon the tis- 
sues under these conditions are 
called exudates, and this phase 
of inflammation is commonly 
called exudative inflammation. 

Let us now look at the 
effect upon a living vascular 
tissues of injury inflicted in 
a different way. 
Injury from Micro-organisms. — Suppose we inject into the ear vein of a 
rabbit a small amount of a pure culture of a well-known and very com- 
mon nicro - organism, Strepto- 
coccus pyogenes. Littlemasses 4 ' * 'T. * *. .* ° '■ ' * '^'^f^ , 
of the living germ will enter ,^.' • • ^ " > ■ ' ^'^^ 
the heart and be driven out S* J .' ■ ! ^ *^/^ *"*'*>. 

again through the arteries in ;-. * ^*; .^ ' . ' -^^i^°o ^^^ 

whose smaller twiglets or in ^ » ^ *' °^ > 3 

the capillaries some of them v'.Vv;. : *A 

will lodge. Here in the living »' ^ ^ > ._. ; ;^ 

tissues the bacteria may find V. v ; ./ . . ■ . .JSS 

good nutrient conditions and '/>r'r : *. >^*^?| 

begin to proliferate, increasing ;,'./^ ^ . ^ ''' ^'^'.^-^^ 

so rapidly in number that they , v - ^ - ^ ; ;?^ ■ ' /'' V * * ' •' ' H^ 
may distend the vessels in * ':"v/^^ ^ \ , * ; «" "^ /' '"^ 
which they lie. If after twenty- ^*^:^^^^>^#^: . " ° '■■,- - ^ " ^ ^ ^. '\^^'^' 
four hours the animal be killed, 
and one examine the organs in 
which the bacterial emboli have 
caught and grown — in the liver, 
for example — he finds small 
blood-vessels here and there distended with bacteria. But the paren- 
chyma and interstitial tissue about them appear to be intact (Fig. 39). 

' Tlioma has shown by similar studies on warm-blooded animals that the reaction 
to injury is in them essentially similar to that in the frog. 



Fig. 40. 



-Bacterial Embolus in 
Necrosis. 



THE Liver with 



The bacteria are still largely confined to the vessel but 
a few are outside. There is a ^one of necrotic liver cells 
about the growing mass of cocci. 



314 INFLAMMATION. 

If, how ever, the ainiiial be allowed to live longer — say two or three days 
— before the examination, the condition of the tissue about the growing 
bacterial mass in the typical course of events shows marked and signifi- 
cant alteration. Immediately around the bacteria the nuclei fail to take 
the nuclear stains (Fig. 40) ; the cytoplasm is unusually granular or 
fallen into fragments. These are the marks of cell death, and from the 
situation of this area of dead tissue about the colony of growing bacteria 
we may infer — and the inference is confirmed by a host of tests and ob- 
servations — that, in growing, the bacteria have set free in the tissue about 







KHi^-:.,'./ 



i";f'*rv 



:.*'-r#;' 



" ' '" ^■^■' v''ii8';> - -sij-fisg^"' -^i^-%i"^- -i^l^-'-^P isS5?;-^sa^i* i^i^ifeto-ftifi^is^- ■>^* •■ -A-:ive 

Fifi. 41.— Necrosis and Suppuration in the Liver from Bacterial Infection— Exudative and 

Necrotic Inflammation. 

The bacteria are scattered in masses, the liver cells about them are necrotic, while leucocytes have 
gathered In large numbers within the necrotic area. With slight further disintegration this mass of deai 
liver tissue and pus cells would form an abscess. 

them some chemical substance whose presence is incompatible with the 
continuance of the life processes in the liver cells, which in fact has killed 
them. 

But very soon the tissues near by show a different sort of reaction to 
this active poison set free upon the spot. Leucocytes gather on the bor- 
ders of the necrotic area and may form a dense ensheathing mass about it 
(Fig. 41). If we look for the origin of these, we find that close outside 
the area of dead tissue and among the gathered leucocytes the smaller 
blood-vessels are dilated, overfilled with blood, and such marks of the 
emigration of leucocytes as a tissue removed from the animal and pre- 
pared for examination may show are unmistakable. Not infrequently 



INFLAMMATION. 115 

extravasated red blood cells and fibrin and a distention of the tissue 
spaces with fluid still further characterize the process as exudative in- 
flammation. 

It was observed in the exposed mesentery or bladder of the frog that 
the leucocytes, once outside the vessels, wandered off in various direc- 
tions in the tissues, some to the surface, some to the lymph-vessels, and 
some far from the veins or capillaries from which they emerged. Xot so 
here. The extravascular leucocytes gather close in the border zone of 
the necrotic area or enter it. And we may usually see in the outer parts 
of such an area of dead tissue scattered leucocytes which are themselves 
undergoing changes indicating the death of the cell. The changes which 
have just been described as the result of experiment in the animal are 
practically identical with those occurring in man as the result of acci- 
dental inoculation. 

If the process continue, one may find on later examination that the 
dead-tissue mass has softened, the bacteria are scattered, and the whole 
central portion may be occupied by a grayish or yellowish grumous or 
fluid mass of dead cells, cell detritus, albuminous and fatty granules, 
bacteria and leucocytes in various stages of necrosis and disintegration. 

Such a localized result of exudative inflammation with death and dis- 
integration of tissue is called an abscess ; the material which it contains 
is called pus. ' 

The changes by which, if the animal survive the formation of abscess, 
the active processes are brought to a standstill and repair is effected, we 
need not now follow. But it concerns us here to appreciate that this is 
a type of one of the most important phases of the inflammatory process ; 
a phase in which a poison produced in the body by the metabolism of 
micro-organisms incites a complex train of active and passive tissue 
changes. 

In our study of illustrative phases of inflammation we now turn to 
the processes by which repair of injured tissues, after more or less in- 
volvement in the inflammatory x^henomena, are brought about. 

Resolution in Inflammation — Phagocytes. — In many cases of exudative 
inflammation, after the subsidence of the active changes in the blood- 
vessels, the exudates are entirely absorbed, and the tissue returns to its 
normal condition ; this is called resolution. Under certain conditions, on 
the other hand — for example, in the case of a wound with loss of sub- 
stance, or in an acute exudative inflammation of a serous membrane 
in which the surface is deprived of its normal mesothelial ^ covering, or 
in the healing of an abscess — new tissues may be produced through the 
agency of old cells or of new cells formed in the inflammatory process. 

^ For a more detailed consideration of suppuration and the characters of pus see p. 
ITo et seq. 

•^ The morphological resemblance of the flat cells covering the surfaces of the great 
serous cavities— peritoneal, pleural, and pericardial— to the endothelium of the blood 
and lymph-vessels has led to their being also called endothelium. But their genesis as 
well as certain physiological capacities which they still retain, render more fitting the 
name mesoihdium. See reference to Minot in footnote on p. 295. 



116 



INFLAMMATION". 




Before considering the waj^ in whicli repair of a wound is effected, we 
shall look at an important class of cells in the body by which foreign and 
^ . ,.^., waste substances are disposed of. 

Phagocytes. — The disposal of small foreign 
particles which in one way or another get into 
the body, and the removal of dead and useless 
fragments of tissue which may be present as the 
result of injury or disease, are cared for by 
larger and smaller cells, called phagocytes. To 
a certain extent the same occurs in the wear and 
tear of normal life. The cells having this mat- 
ter in charge are largely leucocytes (Fig. 12), 
and all are apparently mesodermal, lowly or- 
ganized cells. Some of them are large cells and may be multinuclear — 
the so-called ^' giant cells" ' (Fig. 13). Endothelial cells may also play 
an important role as phagocytes. 

The disposal of dead or foreign material is in part accomplished by its 
being taken into the bodies 



Fig. 43.— Phagocytes. 
These are leucocytes which 
have taken particles of pigment 
into their bodies. 



^5-^5^^ ^ \ 



(i) 



c- 



e 






^ 



n 







^ 



c 







I 



^ o 



o f « 

9 


t 



"'^e- 






^M 



u 



^ 



o 



^^ C 



\0 



of the phagocytes. These 
may either retain it more 
or less permanently, or may 
absorb it in virtue of their 
metabolic powers, or, in the 
case of leucocytes, may carry 
it off to some region of de- 
posit by the exercise of their 
amoeboid capacities. On the 
other hand, the leucocytes, 
and possibly other mesoder- 
mal cells, may either with 
or without disintegration 
develop ferment substances 
which render albuminous 
materials soluble, so that 
dead or useless tissue frag- 
ments may be dissolved and 
carried off in the tissue fluids (Fig. 11). This phagocytic action of meso- 
dermal cells is believed to have an important bearing upon immunity 
and recovery from infectious diseases (see p. 168). 

^ These giant cells may be formed either by the fusing together of endothelial or 
connective-tissue cells, or by a division of nuclei and increase in the cytoplasm of con- 
nective-tissue cells, without a further division of the body. The possibility must be 
recognized that giant cells may be formed also by the fusion of leucocytes.^ 

Giant cells are frequently present in granulation tissue whicli is forming simultan- 
eously with the absorption of some foreign substance or considerable quantities of dead 
tissue (Fig. 43). 

For a study of giant cells, with bibliography, consult HeMoen, Jour. Exp. Med., 
vol. iii., p. 21; see also Fuerst, Ziegler's Beitrage, Bd. xxiv., p. 440, 1898. 



Fig. 43.— Giant Cells. 

The giant cells are at the border of a layer of granulation 
tissue formed about a mass of dead fibrous tissue which is 
being absorbed. 



INFLAMMATION. 



117 



The Healing of Wounds. 

The way in which new inflammatory tissues are formed may be best 
understood by following the process of healing in a wound with loss of 
substance — for exami^le, in a wound through the skin or a mucous mem- 






♦sT' 




fmmk- 



;i^' ?■-*" :*^. •!;• ; ^-'.-Tjft^'*, '--'^^■■'■'s-r:9 *^,:'v;:;^^a 



Fig. 44.— Fragments of Necrotic Muscle^ in process of Absorption under the action of 

Phagocytes. 

brane into the tissue beneath. At first there may be hsemorrhage. After 
this has ceased, the injury to the tissue, the unusual exposure of deep- 
seated parts, the presence of foreign substances, etc., may induce ^he 
same series of events which we have seen occurring in exudative inflam- 







Fig. 45.— Granulation Tissue from Wound of Tongue. 

Early stage with very thin-walled blood-vessels, leucocytes, and young connective-tissue cells. There are 

few intercellular fibrils. 

mation with production of serum, fibrin, and pus. The blood-vessels 
dilate, the circulation becomes slower, serum transudes, and emigration 
sets in. Certain of the cells and fragments of intercellular substance 
near the seat of injury may die, and in time are cast off or are disinte- 



118 



INFLAMMATION. 



grated or dissolved and absorbed or otherwise disposed of by phagocytes. 
The tissue may become soaked and swollen by the transuded serum, and 
the connective -tissue cells in the vicinity may undergo proliferative or 
degenerative changes. 

Granulation Tissue. — After a variable time, usually on the second or 
third day if all goes well, the surfaces of the wound may be more or less 
covered with tiny red nodules called granulations. These granulations 
contain numerous thin-walled blood-vessels which have sprouted out 
from the old vessels near the seat of injury, and around these a new 
loose, succulent tissue is formed, largely, it is believed, from prolifer- 
ation of connective -tissue cells. This is called granulation tissue (Fig. 
45). On the surfaces of the granulations are usually pus cells in vary- 











Fig. 46.— Granulation Tissue from Wound of Skin. 
The walls of the blood-vessels are thicker and Intercellular fibrils are foniiing. 

ing quantity, or the granulations may be more or less covered with 
dried exudate. The way in which the new blood-vessels form by proto- 
plasmic sprouts from the old, and the manner in which connective 
tissue develoi^s from older connective-tissue cells have been already de- 
scribed in the section on Regeneration. Let it suffice here to say that 
the cells of the granulation tissue are at first mostly small and si)her- 
oidal or polyhedral, and are usually packed closely together with only a 
small amount of fluid intercellular substance. Presently some of the 
cells become larger and i)olyhedral, elongated, fusiform, or branched, 
and after a while a delicate, fibrillar intercellular substance makes its 
appearance about them and grows more and more abundant (Fig. 46). 
These larger, variously shaped cells, which appear to be formed out of 
the small spheroidal or indifferent cells of the granulation tissue, are 
usually granular, and the nucleus is generally large and distinct. Some 
of these larger cells which seem to be more or less directly concerned in 
the formation of intercellular fibres are called fhrohl a sts (Fig. 47). 



INFLAMMATION. 



119 



As the granulation tissue grows, new, small spheroidal cells are gath- 
ering by proliferation or by continued emigration. Some of these par- 
ticipate in the formation of the granulation tissue, while others, not find- 
ing conditions suitable for their fur- 
ther development, or even for their .: . — _^— _-^_ 
continued existence, die and pass off - 
on the surface, together with some T 
transuded fluid, as pus. a :f 

The polynuclear leucocytes do not 
apparently share in the formation of ^^!^^ . I? 

new tissue. Whether this is largely ' - ^ 

or wholly derived from small spher- 
oidal cells which may result from 
proliferation of old connective-tissue 
cells, or whether, as is now confi- 
dently claimed by many observers, the emigrated lymphocytes, assum- 
ing the characters of ^^ plasma cells" (see page 103), may be also con- 
cerned, is not yet certain. 

Cicatricial Tissue. — The new tissue gradually becomes more and more 
dense, the intercellular substance more abundant, while the cells decrease 
in number and become flatter and less conspicuous. The epithelium may 
now grow over from the sides, forming by mitosis from the old epithe- 
lium at the edges of the wound (Fig. 48), and finally cover the ne^ 
vascular tissue. The new tissue, having at last undergone more or less 
shrinkage, with atrophy of the blood-vessels, consists of a dense, firm 



Fig. 47.— Fibroblasts or New Connective 
Tissue in a Healing Wound. 

There are numerous new-formed intercellular 
fibrils. 






^^. 
' ^-.-- 



"^P^^/yy 
















Fig. 48.— Healing Wound in the Tongue of a Dog. 

There was loss of substance- muscle, fibrous tissue, and surface epithelium. The lost tissue has been 
replaced by the vascular granulation tissue which is oldest and most dense in the deeper portions, while on 
the surface is a layer of tissue detritus, pus cells, etc., partly dried and forming a scab over the granulations. 
New epithelium is pressing forward from the old at the edges over the surface of the new-formed tissue. 



mass composed largely of fibrillar basement substance with a few flat- 
tened cells (Fig. 49) ; and with this, which is the cicatrix, the healing is 
complete. 

Variations in the Healing Process.— Although in the production of new 
tissue in connection with or following exudative inflammation essen- 



120 INFLAMMATION. 

tially the same processes are involved iu all cases, there are yet very 
raarked differences in the degree in which the different factors share. 
Thus the vascular and exudative phenomena may predominate and very 
large quantities of serum, fibrin, or pus collect, while the amount of 
new-formed tissue may be insignificant. The production of a large 
amount of exudate, particularly of i3us cells — suppuration — usually 
marks the i)resence of micro-organisms whose locally elaborated poisons 
complicate or retard the healing process. In other cases the formation 
of new tissue is the dominant feature, and the production of exudates 






X. 






Fig. 49.— Cicatricial Tissue from Healed Wound. 

seems to be almost entirely subordinated to this end. The process of 
repair which is complicated by exudative inflammation or effected only 
by the gradual formation of a considerable amount of new tissue is called 
by surgeons healing by ^^ second intention." 

The distinction between healing by first and second intention, which 
is of practical imj)ortance in surgery, is, from the pathological stand- 
point, only a quantitative one : for the restitution of the parts to the 
healthy condition is in both cases brought about by exudation, and 
proliferation of cells usually under the influence of vascular changes ; 
but in one case the latter changes are very slight, in the other more or 
less extensive. 

A good deal of variation is frequently seen in the formation of granu- 
lation tissue in the healing of wounds, as well as under other conditions. 
Thus sometimes the body cells respond but feebly to the unusual 
conditions, and neither cell i)roliferation nor blood-vessel growth is 
active. On the other hand, the development of blood-vessels may be 
excessive, while other tissue formation lags. Under these conditions, 
loops and tangles of thin-walled, contorted new vessels may project 
from the granulating surface, while useful tissue formation remains in 
abeyance (Fig. 50). The result of this disproportionate growth of ill- 
formed blood-vessels is the exuberant granulations which the surgeon 
frequently removes from unhealthy healing surfaces. 

Cavities formed by abscesses or by necrosis in any part of the body 
may be filled up and their sides drawn together in a cicatrix, by the 
formation of a provisional mass of granulation tissue similar in charac- 
ter to that which grows in external wounds. So, similarly, cysts may be 



INFLAMMATION. 121 

obliterated aiicl ulcers partially filled and drawn into cicatricial healing. 
Large free surfaces, like the pleura and the peritoneum, may, through 
the intervention of granulation tissue, pass from the denuded condition 
of an active exudative inflammation, either with or without adhesions, 
into a condition which, though by no means a return to the normal, we 
yet designate as repair. 

The so-called organization of a thrombus in a blood-vessel is brought 
about by processes practically identical with those which have just been 
described in the formation of new tissue in reparative inflammation in 
an external wound. The endothelial cells of the vessels and the con- 
nective-tissue cells in their walls proliferate, new blood-vessels develop 
by sprouts from the already existing smaller vessels in their walls or 
close about them. The new cells and new blood-vessels thus derived 



(- 



.^* 



Fig. 50.— Exuberant Granulations. 

From the inner surface of a granulating ovarian cyst containing pus. The tissue between the new capil- 
laries is ill-formed, oedematous, and with few cells, most of which have undergone fatty degeneration. 

gradually penetrate the clot forming new connective tissue, which re- 
places step by step the fibrin and blood which are gradually absorbed or 
removed by phagocytes. 

The part which the thrombus plays in its so-called organization is 
thus a wholly passive one. It acts only as a temporary supi)orting text- 
ure for the development of the new tissue derived from other sources 
which step by stejD replaces it. 

Hyperplasia and Interstitial Inflammation. 

Hyperplasia of the fibrous interstitial tissue of the internal organs and 
other parts of the body — as, for example, in the liver, kidney, heart, 
nervous system, etc. — is of frequent occurrence and is usually associated 
with changes in the parenchyma. In some cases the formation of fibrous 
tissue clearly follows evident and often acute inflammatory processes and 
bears the same relation to antecedent reaction to injury that the cicatrix 
in a healing wound does to the granulation tissue from which it is 
formed. In other cases it is associated with long-continued hypersemia— 



122 INFLAMMATION. 

chronic congestion — of the organ involved. Again, gradnal hyperj)lasia 
of the interstitial tissue appears to take place by the slow increase of 
cells and stroma, without evidence at any time of an active cell prolifer- 
ation or marked involvement of the blood-vessels. Finally, hyperplasia 
of the interstitial tissue may be secondary to damage to or atrophy of the 
parenchyma, as in the spinal cord after degeneration in nerve tracts or 
in the heart after damage to the muscle fibres. In such cases it is often 
spoken of as replacement hyperplasia. These forms of fibrous-tissue 
hyperplasia will be considered with more detail in the sections dealing 
with the special lesions of the viscera. They have all been usually re- 
garded as marks of inflammation. Some of them uncxuestionably are 
so; concerning others, doubt will continue until our knowledge as to 
their excitants considerably increases. In the mean time the term/&>o- 
sts is sometimes applied to the results of fibrous-tissue hyi^erplasia, thougli 
this is still most commonly included among the inflammatory processes. 
Those important phases of inflammation which are due to damage 
from special forms of micro-organisms will be considered in detail in the 
chapter of this book devoted to the Infectious Diseases. ' 

Special Phases of Inflammation. 

The several phases of the inflammatory process, which we have now 
considered, are fairly typical of the reaction of the living body to various 
forms and degrees of injury. If we look at them together and seek to 
gather their dominant features, we find that the changes, varied as they 
are in character as well as in degree, are mostly of three kinds : first, 
those involving a greater or less amount of degeneratio7i or necrosis ; sec- 
ond, those involving local disturbances of the circulation, as well as 
alterations in the distribution and character of the fluid and cellular 
elements of the hloo^— exudative changes -, and third, regenerative, x^roduc- 
tive, or reparative changes. 

Of these three groups of alterations in inflammation those involving 
the blood-vessels and their contents are, in a clinical sense, most striking 
and characteristic, and to many seem to dominate the inflammatory proc- 
esses. But in fact all are closely associated. The various phases of 
inflammation depend upon the nature and extent of the injury, the in- 
herent reactive vigor of the cells, and the character and position of the 
tissue involved. 

Special names have been attached to various forms of the inflamma- 
tory process, descriptive of the feature which from the particular stand- 
point of the observer seems most striking or important. Some of the 
names are descriptive of clinical symptoms, some express the duration 
or character or situation of the lesion, some seek to imjDly more or less 
well-founded views of the nature of the process. Thus among the forms 

' For a suggestive and interesting consideration of the relationship between inflam- 
mation and various forms of "fibrosis" see Adami, Middleton Goldsmith Lectures, Med- 
cal Record, March 14 and 21, and April 4 and 11, 1896, 



INFLAMMATION. 123 

of exudative inflammation those in which the extra vasated serous fluid 
is the most marked feature are often named serous inflaTnmaUons. If 
fibrin predominate, it is called fibrinous ; if associated with much blood 
extravasation, it is termed Juemorrhagic. When the agencies are present 
which induce the necessary vascular changes and x^romote the emigration 
and gathering, and often the destruction, of leucocytes in considerable or 
large numbers, we have a suppurative or purulent inflammation. If much 
tissue death be associated with the process, it is named necrotic inflam- 
mation. 

Again, if certain mucous membranes or mucous glands be subjected 
to the inciting agencies, they may respond by an overxDroduction of 
mucus as well as by an increase or death of cells ; this is mucous or 
catarrhal inflammation. Finally, these various forms of exudate may be 
produced simultaneously, whence arise such compound designations as 
sero-purulent, muco -purulent, etc., inflammation. Inflammation with the 
formation of new tissue is called productive or reparative. 

Local inflammation, especially when incited by micro-organisms, is 
often associated with systemic infection due to a distribution of the in- 
citing agents through the body. This condition will be considered in the 
chapter dealing with the Infectious Diseases (see page 179). 

It has seemed wise to many to attempt to draw a shariD distinction 
between those phases of inflammation which involve only the degener- 
ation of tissues or the redistribution of already formed tissue elements — 
— serum, fibrin, and blood — and those phases which are productive or 
reiDarative. But while this attemxDt aims at the recognition of a biologi- 
cal distinction of fundamental imxDortance, it encounters the great x^rac- 
tical difficulty that both x^hases of the reaction of tissues to injury, the 
exudative and the x^roductive, occur together, so that none of the named 
classes of inflammation represent simxDle and unmixed forms of tissue 
reaction. The important thing is to conceive, as clearly as our knowl- 
edge permits, the nature of the x^rocesses which underlie these various 
manifestations of disturbed cell function and their associated tissue 
alterations. Then the names may serve useful temx^orary ends at least, 
without implying too much or concealing too little knowledge. 

Survey of the Inflammatory Process and its Significance. 

If now, from the vantage-ground which we have won by our survey 
of various typical phases of inflammation, we seek to gain an insight into 
the forces which dominate the varied processes, we note at once that 
from first to last the cell and tissue x^erformances in inflammation, how- 
ever exaggerated or perverted, are only the expression of x3hysiological 
capacities which belong to the structures involved. Thus the contrac- 
tions and dilatations of the vessels are paralleled in health. The exuding 
of fluids through their walls occurs by processes akin to those by which 
blood pressure, osmosis, and selective filtration in endothelial cells main- 
tain the initial circulation into and through the tissue sxDaces. Emigra- 



124 INFLAMMATION. 

tion is a physiological process which we find excessive here, because there 
are structural alterations in the walls of the vessels which permit a freer 
exit of the cells, and because there are also present new and active 
chemical agents which, just as in normal conditions though in exagger- 
ated fashion, excite and control the movement and direction of the leu- 
cocytes. The healing i^rocesses, complex as they seem to be, are actually 
but a rehearsal under unusual and often difficult conditions of cell and 
tissue formation, which is characteristic of the normal period of develop- 
ment. Phagocytosis is a factor of the greatest importance in the normal 
as well as in these abnormal performances of the body cells. 

The degenerative phenomena, among which must be reckoned the 
formation of fibrin, are, as we have seen, incidental rather than primary 
factors in inflammation. 

Thus in all the manifold manifestations of abnormal cell performance 
in inflammation we find no new functions, no new cell capacities. 

We are now brought face to face with the final question : What does 
inflammation mean? 

In those phases which involve the repair of wounds and the regener- 
ation of lost tissues it is not difficult to recognize conservative and bene- 
ficial processes. But how is it with those phases of inflammation in 
which the blood-vessels are largely involved and exudates formed — 
serum, fibrin, and pus? Are we to be contented here with a simple sum- 
mary of the iDhenomena and with the recognition that these are the results 
of exaggerated or physiological cell and tissue performances in the face 
of injury? Or, on the other hand, is there reason for the belief that 
these abnormal manifestations of cell life in the presence of an unusual 
and deleterious environment may, after all,, be in the main conservative 
in their nature, and, even as normal cell functions do, tend — within the 
limitations of an emergency — to the w^elf are of the individual ? 

In the hope of gaining some light upon this question let us look a 
little more closely at the part which the exudates play in exudative inflam- 
mation ; and first at the leucocytes. 

It ^as through the painstaking and brilliant studies of Metschnikoff ' 
that attention was directed to the importance in this connection of com- 
parative studies upon the comportment of lower forms of life in response 
to injury. 

It was found that amoeba, one of the simplest of organisms, when cut 
in two may undergo complete restitution of the part containing the nu- 
cleus, provided the latter be uninjured. The remaining portion may 
live for a time, but ultimately dies. Furthermore, it was found that 
amoeba and other lowly forms of living beings are capable, by the use of 
their simple digestive processes, of destroying micro-organisms which are 
taken into their interior and which might otherwise damage or kill them. 
Thus it was established that the digestive mechanism may become pro- 
tective in lowly organized cells. 

Eising in the scale of living beings, it is found that in forms in which 
^ Metschnikoff, " Comparative Pathology of Inflammation," English translation, 1893. 



INFLAMMATION. 125 

considerable differentiation of some of the cells has taken place, whether 
there be a distinct circnlatory apparatus or not, certain other cells are 
left in a more primitive state : these are phagocytic and can ingest or 
otherwise destroy deleterious material. 

When we come to man and other warm-blooded animals, it is upon 
the leucocytes which have retained so many of the capacities of undiffer- 
entiated protoplasm that attention is esiDCcially concentrated. It has 
been found, as we have already seen, that the movement of leucocytes 
may be directed toward (sometimes from) chemical substances set free 
in their vicinity. This chemotaxis is frequently manifested in the 
vicinity of dead cells or tissues which are the seat of destructive me- 
tabolism. But it is especially in relation to micro-organisms of various 
forms that chemotaxis in the leucocytes is of the highest significance to 
us here. 

Highly virulent micro-organisms may for a time repel the leucocytes, 
probably through negative chemotaxis, but these may later approach 
them. On the other hand, leucocytes most often migrate toward bacteria 
which have gained entrance to the body. It has been proven that leuco- 
cytes, especially the poly nuclear neutrophiles, less frequently large 
mononuclear forms, may take into their interior and destroy living 
bacteria. Dead bacteria also, as well as other inert material, they can 
engulf and destroy. 

This capacity of leucocytes and other mesodermal cells — endothelia, 
etc. — to take up living bacteria and kill and digest them was persistently 
and ably urged by Metschnikoff and his pupils as the chief protective 
agency in the body against bacterial incursions, and to these observers 
all the other phenomena of inflammation formerly seemed of secondary 
imx3ortance. But it was soon shown that this extreme view is not correct. 
For it was demonstrated by many observers that the body fluids, espe- 
cially blood serum, is capable of killing bacteria with which they come 
in contact. When, however, this remarkable quality of the body fluids 
was investigated, it was found that it is most ijronounced under condi- 
tions which involve the breaking-down of leucocytes or the liberation of 
the destructive substances into the fluids. It was possible now to demon- 
strate that the leucocytes do in fact contain a germicidal proteid sub- 
stance or substances. These substances, which appear to be closely 
associated with or related to nucleinic acid, have been called ^'alexines" 
or ^^ protective proteids." ' It has been further demonstrated that while 
the eosinophile cells may move toward bacteria, they are not phagocytic, 
but may set free granules which appear to favor the destruction of the 
germs. 

It thus appears that the earlier view of the almost exclusive impor- 
tance of phagocytosis is not sustained, but that even more than in the 
action of living phagocytes the protective agencies are to be sought in 
the body fluids. But it is also clear that the protective capacities of the 
body fluids are the result of cell activities, as indeed might have been 
' For further consideration of this subject see p. 169. 



126 INFLAMMATION. 

inferred in advance of the long line of careful experiments which finally 
led to the demonstration. 

The importance of this protective power of the body cells and body 
fluids is not exhausted with their germicidal action. For not less sig- 
nificant is the role which these may assume in the establishment of other 
phases of immunity to the incursion of micro-organisms. This, however, 
will be considered later in the general survey of the infectious maladies. 

If now one seek for ways in which the other exudates, serum, and 
fibrin may be useful to the indi^ddual, it is obvious that in the dilution 
of locally engendered poisons and in their removal from a vulnerable 
region the fluid may at times be beneficial. Fibrin, too, by closing inflam- 
matory foci, through temporary adhesions, or by the sealing of absorbent 
surfaces, may limit the extension of injurious agents, as is so frequently 
the case in local infectious injuries in the peritoneal and pleural cavities. 
That the regeneration and repair of tissue which may be associated with 
or follow the more active phases of inflammation are, as a rule, beneficent, 
is not doubtful. 

There is, of course, another side to the matter. For new cicatricial 
tissues which have formed in the process of rej^air may be so situated as 
to cause serious impairment of functional performance or even fatal 
strictures. The gathering of leucocytes, too, may be so excessive and 
their proliferation so extreme as to lead to delayed healing or to serious 
exhaustion from suppuration. But notwithstanding these irregularities 
and failures there seems to be good reason for the belief that, on the 
whole, the processes involved in inflammation are conservative, and, 
within the limitations which may be set by the varied and changing con- 
ditions of injury, tend to maintain the welfare and sustain the life of the 
individual. 

CHARACTERIZATION OF THE INFLAMMATORY PROCESS. 

The general conception of inflammation which we have just set forth 
looks beyond the gross manifestations of disordered function and altered 
structure, by which it was originally marked, and beyond the complex 
and varied expressions of aberrant cell activities, with which our later 
science has mostly dealt, to the fundamental qualities of living substance. 
And thus at last, with the heart of the subject in view, a characterization 
of inflammation becomes possible which is suggestive and useful, though 
it may not indeed be final. Perhaps among many such characterizations, 
that of Adami ' is on the whole the most clear and precise, and with him 

1 For a fuller consideration of inflammation from the point of view which in general 
is here adopted, one may consult the excellent article on "Inflammation " by Adami in 
Allbutt's "System of Medicine," vol. i., p. 54. 

In Thonia's work on "General Pathology," vol. i., is a clear exposition of the vari- 
ous processes concerned in inflammation, with a fuller recognition than is commonly 
accorded to them of the mechanical factors involved. In both of these works the more 
Important bibliography may be found. 

For bibliogiaphy and critical resume of studies on pathological organization, in- 
flammation, etc., see Borst. Lubarsch and Ostertag's Ergebnisse, Jahrg. iv., for 1897, 
p. 461. See also references under Regeneration, page 94,' and under Tumors, page 273. 



INFLAMMATION. 127 

we may at present wisely consider inflammation as ^'the local attempt at 
the repair of injury/' The fundamental conception upon which this 
characterization is based is that inflammation is an emergency measure 
incited by injury, in which the body adapts to unusual ends as best it can 
mechanisms and i^owers normally maintained for other purposes. 

This ^'iew of inflammation, however much it may be modified as our 
knowledge grows, recognizes a far-reaching significance in the complex 
processes involved. And while throwing light upon the practical prob- 
lems of the physician, it x)oints the way to a broader conception of other 
abnormal conditions in which also the adaptation of physiological cell 
capacities to new conditions seems to furnish a clew to many manifesta- 
tions of disease as yet but little understood. ' 

Xow that we have gained a conception of the inflammatory processes 
in general and some clews as to their significance, it does not seem neces- 
sary to enter here upon a detailed description of the variations which they 
present, since these are largely influenced by the character of the incit- 
ing agents and by the situation in which they act. Such details as may 
fall within the scope of this work are given in the section dealing with 
micro-organisms as inciting factors in disease, and in the part dealing 
with the lesions of special organs. 

' Consult, for a clear and comprehensive view of adaptation in pathological proc- 
esses. Welch. Transactions of the Congress of American Phj'sicians, vol. iv., p. 284, 1897. 



CHAPTER V. 

ANIMAL PARASITES. 
Protozoa.' 

This class of cellular organisms, which belong close upon the border- 
land between animals and plants, contains many which are parasitic in 
man. Only a few are of known pathogenic significance. There is, how- 
ever, much reason for the growing belief that many forms play an im- 
portant part in inciting some of the serious infectious diseases whose 
etiology is still obscure. 

The protozoa are commonly divided into three groups — Rhizopoda, 
Sporozoa, and Infusoria. 

RHIZOPODA. 

In this group the Amceha coll (Amoeba dysenterica, Councilman and 
Lafleur) is of considerable pathological significance. 

It has been repeatedly found in acute and chronic dysentery, in the in- 
testinal contents, at the bottom 
of the intestinal ulcers, and in 
|, the secondary abscesses, espe- 
/^ cially of the liver, which may ac- 
company ulcerative colitis. The 
amoeba is believed to be the in- 
citing factor in both the pri- 
mary ulcerative colitis and its 
complicating abscesses (see ^. 
511). 

V.^ ■ '^^ The Amoeba coli (Fig. 51) 

' -x^^^^ ^ ^ is a spheroidal cell, from five to 

FIG. 5i.-AM(EBA COLI. eight times the diameter of a 

From the intestinal wall near an ulcer in amoeWc colitis. i'Cd blood Cell, with granular 

IDrotoplasm and a vesicular nu- 
cleus. It often contains larger and smaller vacuoles. Frequently, es- 
pecially when the amoeba is active, a i^ortion of the protoplasm appears 
almost homogeneous — ectosarc — while the rest — endosarc — is granular. 
When moving it assumes various forms, thrusting out and withdrawing 
nearly homogeneous pseudopodia. It may also change its shape without 

1 For a resume of our present knowledge of the parasitic and other protozoa, con- 
sult Mannaherg, Lubarsch and Ostertag's "Ergebnisse der allg. Aetiologie der mensch- 
lichen und Thierkrankheiten," Jahrg. I., Abth. 1, p. 916, 1896; and Kruse in Fliigge's 
"Mikroorganismen," vol. ii. 






AXIMAL PARASITES. 129 

progressive movement. It occurs in acute and clironic dysentery, fre- 
quently in Egypt, occasionally in Russia, and is often seen in the United 
States. ' 

Other species of amoeba have been found parasitic in the human 
intestines. 

SPOROZOA, OR GREGARINiE. 

In this group of the Protozoa some forms of coccidia possess well- 
defined pathogenic i)Owers. The so-called psorospermke — minute oval 
structures about 0.035 mm. long, with a thick 
capsule and coarsely granular contents — which 
are of very frequent occurrence in the liver 
of the rabbit, forming a part of the contents 
of yellowish, irregular-shaped cysts, have been 
found in the liver, in a pleuritic exudate, and 
in the kidney, ureter, and heart muscle in ^ig. 52.-cocciDirM oviforme. 
man. The organism is more properlv called Jrom uvev of rabbit. t^hoNvmR 

^ . . phases in the development of the 

CoCCidium OVifonne (Fig. 52), while the spores psorospermlse, which are seensepa- 

which it forms are termed psorospermicT. ^f" '' "^"^ *^^ "^p'^'^^ ^^ ^- -^"^^ 

Another, smaller form, occurring in the 
intestinal epithelium of dogs, cats, and rabbits, has been found in two 
cases in a similar situation in man. 

Eixf ord and Gilchrist ' have described in detail two cases of x3rotozoan 
(coccidoidal) infection of the skin and other organs, making a careful 
comi^arison between these and organisms somewhat resembling them 
which have been found in various skin lesions. 

Organisms apparently belonging in the group of Sporozoa have been 
found in certain little understood, apparently infectious epithelial cell- 
growths — MoUuscum contagiosum. 

The claim that some of the carcinomata may be caused by Sporozoa 
has not as yet been sustained (see p. 270). 

The PJasmodium mcdarice, the excitant of intermittent fever, is de- 
scribed elsewhere (p. 252). 

THE INFUSORIA. 

These are represented in man by several genera. Their pathological 
significance is not clearly determined. 

Bcdantidlum coJi is an ovoidal organism, from 0.06 to 0.1 mm. long, 
with cilia along the sides, which occurs occasionally in diarrhoeal dis- 
charges : especially observed in northern Euroi)e (Fig. 53) . 

Cercomonas intestinaJis is a pear-shaxDcd, flagellate structure (Fig. 54), 
about 0.012 mm. long, making, when alive, rapid movements. It has 

' We refer for further details concerning tlie Amoeba coli to the work of Councilman 
and Lafleur on "Amoebic Dysentery," Johns Hopkins Hospital Reports, vol. ii., p. 395, 
1891. For a method of differential staining of the Amoeba coli see Mallory, Journal of 
Experimental Medicine, vol. ii.. p. 529, 1897. 

-Johns Hopkins Hospital Reports, vol. i.. p. 209, 1896; Bibliography. 
9 






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¥V(*J-. M. -A^1.^A^>liXV\X?^ tN*ni^«t^\Xtl^ AWM^ n^^wn- 



?*^w<*^^wiv ?^H^*'1^ *^ 'ji^ivfl^'iW K-NS^a^l l^;vnH> *iwiw\ 










Vl^^m 



1 IK 






,1'VJS!<>('S^«(?§ 






.\.»v>,>J^hh>(. >>.,»f*<h."*4». 



&.;ic<;. t.M-M^> -- pr<!flM?vSJ<^ ^''■' '^•'"^ ''"'^ 






AMMAL PARASiITEj* 



131 



r^m ot whuh rh^y attach themselres. Th,.re are .ereral g«^r» and 
.pe««^ found .n man. The most common genus is IHst^^ Of these 
/>. kj<rt,^m IS of most freqneot oeeurrenee (Pig. 5e). It is about 30 
nni. long, and iwualljr oeeurs in the gall duets and g-all bladder The 
embryos *re often attached to water plants, from eating which the 
mf«t.on ,« believed to oeenr. i>. ?„«^^„.» i^ „iore slender, pointed' 

at the ends. S to 10 mm. long, and has been 

f ijond a few tJBaes im the gall bladder J>. giueme 

is a slender worm ab^mt l.> mm. long, and has 
-^n foniwl ill the bite in eon-siderable num- 
•ers. pwrtieiilariy in the Chinese. 1>. titamO^ 
'»» is a more nearly (-ylindrical worm- the 

--xes are distinct ; the male from 12 to U mm. long, the female Id to 




About narurai siae. 



^,^^^1?:^^ 



'J. 



CE3T0DA (T^f^ m»'jm). 
Tb^ important wormi^ eon^, m fc aa^tare state €^' more or k^ 

virftiefe. eall^ the he<id, i» a T^^m^j tmj,^ stria^are for the attaeh- 

M^t of the colony to it5 host. The neck and 
head are calletl the ^e^,^^, while the segiiient^ 
are called pro^mide^. These wm^ have 
neither month nor alimentary canaL They 
ad-e hermaphrodites, the sexes'being united in 
the proglottides. The head and neek (seol^x) 
may exist as an immature form in various tis 
s«es and organs where they are encysted, and 
are often called eysticereu®. 

Tmiin soimm is of fre(|uem occurrence in 
man. It may be sereral; metres in length, and 
may be coileti up or stretched out in the small 
intestines. Several worms may be in the o-ut 
at o©e tiome. The hea^ abom* the a^ of a 
:>ni's head (1-ig. 57). has a projeetiiig probos- 
s or rostellum. around whieh are arranged 
a double row of horny hooklet^ Eelow these 
are four sueking ddses at the sides of the he.id. 
Tlie hooklets of the anterior row are larger 
than tlioee in the poeterior row. and are from 
^.1«5 to t>.18 mm. long. The proglottides, 
when imBj ^e^dioped, are from 1*> to 12 mm 
^fc,,^, ^ , - ^^^- ^^^' ^^^^ ^-^ nearest the head are mu^h 

*^r and nnmarure. The eggs of T. solium are ov^dal stTuetures. 
^^m 0.tK> mm. in diameter. The embryo M tte worm is most eom- 



Li 



and from 



132 



ANIMAL PARASITES. 



/ 



\ 



L 



4 



<r:/. 



Head and Pro- 



Fig. 58.— T^NIA MEDIOCANELLATA 
GLOTTIDES. 

A^ head X about 15. 

B, mature proj?lottid, showinR' generative apparatus. 
G, head and fragments of immature proglottides, show- 
ing gradual tapering of the neck. Natural size. 



moiily seen in the muscles of the pig as aii encysted scolex, commonly 
called a ^^measle." It occasionally occurs in man in the muscles, brain, 
eye, etc., and is called cysticercus ceUulosce. It is usually about the size 

of a pea, but may be as large 
as a pigeon's egg and surround- 
ed by a connective-tissue cap- 
sule. 
I ^ Infection >yith the worm 

I occurs in the human subject 

I from the ingestion of insuf- 

ii nciently cooked ''measly" 
' • pork, or, in the case of cysti- 

c cercus cellulos?e, from the in- 
7 gestion of the eggs, which may, 
/ in a variety of ways in un- 
/ c cleanly persons, get into the 
food. 

Tivnla mediocanellata (T. 
saginata Leuckaet). — The 
head of this species is some- 
what cuboidal, with neither ros- 
tellum nor hooklets, but with 
four sucking discs (Fig. 58). 
The segments are generally broader and shorter than in T. solium, and 
the worm is usually larger. In the embryonal form the scolex occurs 
as the Cysticercus tcenice mediocanellatce in the form of small cysts in the 
muscles of cattle, from the eating of which in the uncooked condition 
the infection occurs. This is the most common tapeworm in the United 
States- 

Tmnia ecJmiococciis. — This worm in the mature condition forms a 
short, small colony inhabiting the intestine of the dog. The head is 
about 0.3 mm. in diameter and 
has a double row of hooklets 
around the rostellum. The pro- 
glottides are three or four in 
number, the last being the larger. 
The entire colony is not more 
than 4 to 5 mm. in length. 
The significance of this parasite 
in human pathology depends 
upon the cysts, called hydatids, 
which it forms, in the immature 
or cysticercus sta.2:e, in various parts of the body. Intimate associa- 
tion with dogs favors the acquirement of this parasite. When the eggs 
of the mature worm get into the intestinal canal of man they undergo 
partial development and find their way into the tissues and organs, 
most frequently into the liver. Here cysts are formed which become 




Fig. 59.— Cuticula of Echinococcus Cyst. 
Showing lamellated structure. 



ANIXAL PARASITES. 



133 




Fig. 60.— Scolices of T^xia echixococcus, x 

In one the rostellum is projected, in the others it is 
withdra\Yn. 



encapsulated by a conuective-tissue membrance produced by the iuflam- 
matory reaction of the organ. 

The cyst wall of the parasite is formed of two layers — an outer, finely 
lamellated layer called the cuticida (Fig. 59), and an inner, granular 
layer, containing muscle fibres and blood-vessels, called i\iQ xmrencliyma- 
tous layer. Inside of the primarj^ 
cyst secondary cysts sometimes 
form, called daughter cysts, and 
within the latter tertiary cysts, 
called granddaughter cysts, may de- 
velop. On the inner surface of the 
cysts, either primary, secondary, 
or tertiary, the scolices or heads 
of the immature worm are formed. 
These develoi) in the walls of the 
pediculated vesicles called brood 
capsides. The walls of these vesi- 
cles have a lamellated cuticula and 
a i^arenchymatous layer similar to 
those of the x)rimary cysts. The 
scolices, of which there may be 

several in each brood capsule, are similar to the heads of the mature 
tapeworm. They are about 0.3 mm. in diameter, having a rostellum 
surrounded by a double row of hooklets and four sucking discs fFig. 
60). At the posterior end of the scolex is a pedicle by which it is 
originally attached to the wall of the brood caj)sule. Little, lamellated 
concretions of lime salts are often present in the scolex. The anterior 
portion of the scolex, the rostellum, hooklets, and suckers, are often 
iuvaginated in the posterior portion. The scolices may be free inside 
of the brood capsules, or, owing to the rupture of the latter, they may 
be free in the cavity of the primary cysts. They may die and degen- 
erate, forming a granular mass in which the hooklets may be embedded, 
or the hooklets may be free in the brood ca]3sules or in the primary 

cysts. Sterile cysts are often found, that 
is, those in which neither brood capsules 
nor scolices are developed. 

The cysts contain, in addition to the 

scolices, a clear, gelatinous fluid. This 

fluid may become turbid by admixture 

with disintegrated scolices or fragments 

of the parenchymatous layer, or it may 

contain fatty detritus, cholesterin crystals, 

and particles of lime salts. The fluid may 

be partially absorbed, leaving a thick, 

grumous material within the cysts, which may become calcified or 

converted into a stony mass. ^ATien the scolices are not found entire 

the diagnosis may be made by the discovery of the separate hooklets 




Fig. 61.— Hooklets from Scolex of 
t-enia ecchixococcus. 



134 ANIMAL PAEASITES. 

(Fig. 61) or fragments of the characteristically laniellated cyst walls. 
The connective -tissue walls of the primary cysts may become fatty, oj' 
caseous, or calcified. 

Sometimes the secondary vesicles project outward instead of inward, 
forming a series of cysts outside of the primary one. This variety of de- 
velopment is sometimes seen in man, but is more common in the domestic 
animals. It is called Echinoccocus scolecipariens or exogena. 

Another variety of echinococcus, called E. muUUocularis, is almost 
always found in the liver, and appears to be the result of incomplete 
and disturbed development of the embryos or cysts. It consists of a 
congeries of irregular, usually small cysts (Fig. 323, page 558), surrounded 
by broad and narrow bands of connective tissue, and sometimes contain- 
ing gelatinous fluid and scolices or booklets ; but the latter structures 
are commonly absent or difficult of detection. The whole is often sur- 
rounded by a dense connective -tissue capsule which may be calcified. 
The entire mass often presents an alveolar structure and was formerly 
regarded as a tumor — alveolar cancer. The diagnosis may be established 
by the discovery of the booklets or scolices, or fragments of the laniel- 
lated cuticula. This form of the parasite is rare in America. 

There are four or five other species of tsenia, occurring rarely in man. 

Tcenia nana. — This species occurs in the form of small colonies, about 15 mm. in 
length. The rostellum is surrounded by a single row of booklets. It has been seen 
once in large numbers by Bilharz in the duodenum of a child which died of meningitis 
in Cairo. Tmnia Jlavopunctata. a species about which little is known, is reported twice 
in America as occurring in the intestine of young children. Tcenia madagascariensis, 
also little known and rare, has been seen in two children in Madagascar. 

Tcenia cucumerinct. — This species occurs in colonies about 20 cm. long. The head 
is very small and spheroidal, and has four rows of booklets. It is frequent in the 
small intestines of dogs and cats. It occurs occasionally in man. Its scolex inhabits the 
dog louse, and infection may occur in man by the transference of the lice or the embryos 
of the parasite to the mouth, as the result of the filthy habit of kissing dogs and cats or 
permitting the face to be licked by them. 

Bothriocephalus latus. — This, the largest of the human tapeworms, has very broad, 
quadrangular proglottides. The head is ovoidal and about 2 mm. long and 1 mm. 
broad. It has no proper sucking discs and no booklets, but by long gi'ooves on either 
side of the head the animal attaches itself to its host. Tlie neck is long and filiform. 
It occurs most frequently in Europe, particularly in the northern provinces. The eggs 
undergo partial development in water, and are taken up by the pike and eel-pout, and 
perhaps by other fresh-water fish, from the ingestion of whose flesh in an imperfectly 
cooked condition the human infection occurs. Two other species of Bothriocephalus 
have been described as of rare occurrence in man : B. corclatus in Greenland and Iceland, 
and B. cristatus. 

NEMATODA (Bound Worms). 

These worms are in general cylindrical, elongated, usually pointed at 
the ends, and sometimes filiform. The surface is sometimes smooth, 
sometimes irregularly beset with hairs and papillae, or possesses longi- 
tudinal elevated strise or transverse rings ; but the body is not segmented. 
There is a mouth at the anterior portion, and a ventral anus near the 



ANIMAL PARASITES. 



135 



posterior end. The intestine is straight. The sexes are in most forms 
distinct, the male being in general smaller than the female. 

Ascaris lumbricoides. — This is one of the most common of the human 
intestinal parasites, and is of particularly frequent occurrence in chil- 






EGGS OF Nematode Worms. 



A, Eggs of Ascaris lumbricoides, X about 300. B, eggs 
of Oxyuris vermicularis, X about 250. 



Fig. 62.— Ascaris lumbricoides. About half natural size. 
A, Male. B, Female. After Perls. 

dren. It is of a light -brownish or reddish color. The female is from 30 
to 40 cm. long and from 5 to 6 mm. thick. The male is somewhat more 
than half as large (Fig. 62). Both sexes are pointed at the ends, the 
posterior end of the male being 
curved into a spined hook. The 
eggs, from 0.05 to 0.06 mm. in 
diameter, are surrounded by an 
albuminous envelope (Fig. 63 A) 
and are quite resistant to destruc- 
tive agencies. The ]node of de- 
velopment and life history of these 
parasites are not very w^ell under- 
stood. Their usual seat in man is 
the sinall intestine, but they may 
wander into the stomach, and ex- 
ceptionally get into the mouth, 
nose, bronchi, gall passages, peritoneal cavity, etc. 
in the gut or present in great numbers. 

Two other species of ascaris have been found in man. A. maritima 
was found in the vomit of a child in Greenland, in an 
immature condition. A. mystax, a tolerably common 
form in cats and dogs, has been found a few times in 
man. It is smaller than A. lumbricoides. 

Oxyuris vermicularis (Threadworm or Pinworm). — 
Tliis si^ecies is xqyj small ; the female has a pointed tail 
and is about 1 cm. long. The posterior end of the male, 
which is about 4 mm. long, is blunt, and after death 
somewhat curled (Fig. 64). The eggs (Fig. 63 B) are 
produced in great numbers, are oval, and about 0. 052 
mm. long. This parasite is very common in children, 
and may be present in large numbers in the colon. 
This worm is known to infest only the human subject, and infection 
doubtless occurs by the ingestion of the eggs, which are widely dis- 
tributed in a variety of ways on many objects, fruits, etc. 



They may be single 



A. B. 

Fig. 64.— Oxyuris 

vermicularis. 

A, Female. B, Male 



136 ANIMAL PARASITES. 

Strongylus gigas. — This is a slender red worm, the female being some- 
times 1 metre long and over 1 cm. in diameter. It has been found 
several times in the pelvis of the kidney in man. It is more common in 
the wolf, fox, horse, seal, and some other animals. 

StrongyJus longevaginatus. — The female is about 2.5 cm. long, the male, 
as usual, shorter. It is of a yellowish-white color, and has been found 
once in the lung of a boy in Germany. 

Strongglus siihtiUs. — A very small species (female 5.6-7 mm. long) has 
been described by Loos as occurring in Egypt in the human intestine. 
But it is believed to be without pathological significance. 

Dochmlus duodenaUs ( Ankylostoma duodenale). — The female is from 
1 to 2 cm. long, the male about 1 cm. long. The body of the male is 
dilated anteriorly and curved backward. Its mouth is furnished with 
a chitinous capsule and chitinous claws and teeth. It is found in the 
small intestine of man in Italy, Switzerland, Egyi^t, and Brazil. The 
head is burrowed into the mucous membrane of the host, and the animal 
is nourished by the blood which it sucks out, and which is usually seen 
in its intestine. An ecchymosis is i^rbduced at the point of attachment, 
or even severe haemorrhage, and marked anaemia may be the result of 
the presence of large numbers of the parasites. 

TricJiocejjhcdus dispar (Whipworm.) — The males and females are of 
nearly equal size, 4 to 5 cm. long. A little less than one-half of the 

body (the posterior portion) is about 1 
mm. thick, and in the male is rolled into 
a flattened spiral, but in the female is but 
slightly bent. The anterior part of the 
body is very slender (Fig. Qq) and is em- 
bedded in the mucous membrane of the 

FKx. G5.~TR1CH0CEPHALUS dispar. 1 J. mi i x j i 

host. The eggs are elongated, oval- 

From the skin of the mons veneris. 

shai:>ed, about 0.05 mm. long and about 
one-lialf as wide, with a thick brown capsule. This parasite is very 
common in some countries, especially in France and southern Italy. It 
is commonly found in the caecum, usually in small, but sometimes in 
very large, numbers. It is generally of little pathological significance, 
commonly producing no symptoms. Its developmental history is not 
w^ell known. 

Trichina spircdis. — The female of this common parasite is, in the ma- 
ture condition, about 3 mm. long, the male from 1 to 1.5 mm. long; they 
are filiform in shape and white in color. The young are born in the 
form of tiny worms about 0.01 mm. in length and somewhat similar to 
the adult in shai)e. Infection occurs in man from the ingestion of in- 
sufficiently cooked pork. The muscle of the diseased pig contains the 
embryos of the parasite in an encysted condition. In the stomach the 
capsule of the worm is dissolved and the embryos are set free. They 
very rapidly mature, increasing in size, and the females give birth in 
the small intestine to very large numbers of young. It is estimated that 
a single female may give birth to from 1,300 to 1,500 young. These find 




established ; probably they 


traverse 


the 






J 


^It/-" 






^ n : 


t 


^^^_^- 




. ^ ^ 


/ t. t 




^ "" \ 


1 


' r 


i^^ :;;> 


' 'i 




^j' 


</^i^\ -:::<r/f 


1 




«/ 


' fv"^^' 


> 




4' 


J 


/ /^ c^^£^ 


'^^\ 


^ 13 




*0 ^ 


^ f /,/ * 


V \^ 


■— -^^^^J- 


A::, 


; ^'^ I ^' 


^ "5''/ 


/ 








f 




, : :•)?" 


3 


4 




'"/ 


,>\' -^J 


d 


-■, ' 






. ({^ 










at.- ^ 








Fig. 


66.— TRICHIiNA SPIRALIS 







ANIMAL PARASITES. 137 

their waj^ through the mucous membrane and wall of the gut, into vari- 
ous parts of the body. 

The exact course which they take in getting out of the gut is not fully 

tissues in different ways. At 
any rate, they find their way 
to the voluntary striated 
muscle tissue, which they 
penetrate, and enter the 
V muscle fibres. Here they 
cause a disintegration of the 
contractile substance, and 
coil themselves inside of the 
sarcolemma. In this situa- 
tion they become encapsu- 
lated by material in part 
furnished by themselves, in 
part by means of the inflam- 
matory reaction which their 

Tbe parasites are encysted in muscle. In one capsule the presence induceS in the COU- 
pjjraslte has died, and the granular material replacing it is cal- ^^^.tive tisSUC of the mUSClC. 

The worms are surrounded 
inside the capsule by granular material (Fig. 66). The ca^DSule after 
a time becomes partially calcified, and in this condition may be readily 
seen by the naked ej^e as a tiny while speck. In this encysted state they 
may remain inactive but living for an indefinite, often for a very long 
time. Most frequently the cysts contain but one embryo, but they may 
contain from two to four. The embryo may die and its remains become 
calcified. 

The same course of events follows when the muscle trichinse are eaten 
by the pig or a variety of other animals. 

The embryos in the muscle are killed by a temperature of 55° C. and 
by some of the methods of curing pork. 

The embryos may mature and a new generation be born within from 
five to eight daj^s after the ingestion of the diseased meat. 

At the result of the presence of these parasites in the body, if the 
invasion be severe, nutrition may be impaired and catarrhal enteritis, 
broncho-pneumonia, hyx)erplasia of the mesenteric lymph nodes, and fatty 
degeneration of the liver may occur. Leucocytosis with a great increase 
in the number of eosinoi^hile cells is common. The encapsulated em- 
bryos may be found in enormous numbers in ^ arious voluntary muscles 
of the bodj^, but they are most apt to be found, when not very abundant, 
in the muscles of the neck and larynx, in the intercostals and the dia- 
phragm. They tend to collect toward the tendinous extremities of the 
muscles. Trichinae also occur in the rat, cat, mouse, and other animals. 

Filaria medinenis (Guinea worm). — This is a thread-like worm; the 
female, which is alone known, being sometimes as much as 80 cm. long 
and from 0.5 to 1.7 mm. thick. It is common in the East, and inhabits 




138 ANIMAL PARASITES. 

the subcutaneous connective tissue, in Avliich it often gives rise to ab- 
scesses and ulcers. The embryos live for a time free in fresh water, and 
are then taken up by a species of fresh-water crustacean, in Avhose body 
they undergo further development, and by the ingestion of which the 
^'nfection of the human subject occurs. 

Filaria sanguinis hominis. — The embryo of this parasite, which inhabits 
the blood and lymph of man, especially in Brazil, Egypt, and some parts 

of the Orient, and occasionally occurs 
in this country, is about 0.35 mm. 
long, rounded anteriorly, and pointed 
at the tail (Fig. 67). It has about 
the diameter of a red blood cell. It 

FIG. 67.-FILARIA SANGUINIS hominis.-embrt- ^pp,.,.^ somctimes \\\ ffrcat numbers 
ON ic FORM FROM THE BLOOD. occuis, someiimes m giear numoeis, 

in the blood during the night time, 
being as a rule absent during the day. It may occur in the urine in 
connection with chyluria and hfematuria. The mature female is from 
8 to 10 cm. long, and has been found inhabiting the lymx)h vessels of 
man, particularly in the scrotum and lower extremities. Owing to the 
obstructions which it causes in the lymph circulation, and to the local 
irritation which its presence induces, it sometimes give rise to lymph- 
angiectasis, oedema, abscesses, and perhaps elephantiasis. One of the 
embryonic stages of development is believed to tike place in the body 
of a species of nocturnal mosquito. Through the bodies of the dead 
mosquitoes, which are liable to fall into the drinking-water, it is believed 
that the spread of the parasite may occur. 

There are several other species of filaria occasionally found in man 
which it is not necessary to enumerate heie. ' 

Rhabdonema stro7igyloides. — A small, filiform worm from 1 to 2 mm. 
in length is found, often in enormous numbers, in the intestines, biliary 
and pancreatic ducts of man in Cochin China and in Italy, giving rise to 
endemic diarrhoea. It has been thought that there are at least two 
species, which have been described under the generic name Aguillula, but 
recent researches by Leuckart have led him to believe them to be differ- 
ent developmental stages of the same form, for which he suggests the 
above name. 

Methods of Study of Worms. 

Filaria sanguinis may be preserved by preparing a smear of the blood containing it 
on a slide in the usual wa}^ (see p. 352), and studied after staining with methylene blue. 

The larger parasites may be hardened in formalin and studied whole after dehydra 
tion in alcohol and clearing in oil of cedar or origanum. Or sections may be made after 
embedding, and stained and mounted in the usual way. 

The examination of muscle for trichina is often of great practical importance. For 
this purpose small pieces of fresh muscle are squeezed into a thin sheet between two 
slides, and examined with a low power. A considerable number of bits of muscle should 
be examined, particularly from the above-mentioned favorite situations, before exclud- 
ing them in a suspected case, because they are sometimes present in small numbers. A 

1 For ])ibliography consult Lotlirop and Pratt, Am. Jour. Med. Sciences, vol. cxx., 
p. 525, 1900. 



ANIMAL PAEASITES. 



139 



thorough search is of especial importance in the examination of pork, since, owing to 
the enormous fertility of the parasites, even a moderate number may give rise to a 
severe infection. 

For the minute examination of the parasite, bits of muscle should be hardened in 
Orth's fluid and alcohol, decalcified if necessary, and, after embedding in celloidin, tliin 
sections cut and stained double with hsematoxylin and eosin, and mounted in balsam. 
Bits of muscle may be also teased, the embryos picked out with a needle, and the cysts 
either broken open under a lens with the needle, or squeezed under the cover glass. 
The embryo worm thus set free may be mounted in a mixture of equal parts of glycerin 
and picric acid. The adult forms, which may be obtained b}' feeding rabbits with un- 
cooked trichinous muscle, and examining after the proper interval, may be hardened in 
Orth's fluid, and mounted in a mixture of equal parts of picric acid and glycerin, or 
in the same mixture which has been lightly tinged with eosin. 

Arthropods. 

The scope of this work does not iDermit us to enter in detail into the 
subject of external parasites, which will be fonnd described in treatises 

on diseases of the skin or in the general works on 

parasites referred to below. Bnt, owing to their 

freqnent occnrrence and practical importance, we 

may briefly describe two of the 

more common forms of arthro- 

IDods, the ^4tch insect ^^ and the 

^' louse." 

The common ^4tch insect" 

— ^ar copies hominis (Acarus 

scahiei) is shaped somewhat 

like a turtle, with a chitinous 

covering, and presents the gen- 
eral a]3pearance seen in Fig. 

68. The female is about 0.45 

mm. long, the male a little 

smaller. 
The x)arasite bores little tunnels in the skin, in Avhich the eggs are laid 
and the young hatched. After a few days these bore fresh channels in 
the skin. For their detection a bit of the superficial layer of the skin is 
snipped out with curved scissors, dehydrated and cleared up with oil of 
cloves, and examined under a low power, when the tunnels and the para- 
sites, if present, will be readily visible. 

The head louse, Fediculus capitis, is from 1 to 2 mm. long, the female 
being slightly the larger. The general appearance of the insect is seen 
in Fig. 69.' 

Method of Study of Insects. 

These, if small, may be cleared in turpentine and mounted in balsam, or sections 
may be cut after embedding in paraffin. 

^ BihUogrcqjJiy. — Especially to be recommended for detailed description of human 
and animal parasites is the small work of Moniez, "Traite de Parasitologic," Paris, 1896. 

Consult also, especially for the forms of eggs and other parts of animal parasites 
which may be found in the excreta, von Jaksch, or Simon, or other works on clinical 
mici'oscopy. 





Fig. CS.^Sarcoptes homixis 

—THE "itch insect." 



Female; back view. 
Fiirstenberg. 



After 



Fig. 69.— Fediculus 
capitis — the "head 

LOUSE." 

Male. After Braun. 



CHAPTER VI. 

PLANT PARASITES. 

The plant parasites of man belong among the simplest of living or 
ganisms. Three distinct gronps are of frequent occurrence in or upon 
the body. These are : 

1. Bacteria, or fission fungi (Schizomycetes). 

2. Yeasts, or yeast fungi, or sprouting fungi (Blastomycetes). 

3. Moulds, or mould fungi (Hyphomycetes). 

The first group, the bacteria, is of the greatest significance, because 
it contains organisms which are very frequently the excitants of serious 
disease. ' 

I. Bacteria. 

MORPHOLOGY, PHYSIOLOGY, AND DISTRIBUTION. 

Bacteria are minute unicellular plants devoid of chlorophyll, multi- 
plying by transverse fission and in some cases preserving the species by 
the formation of spores. 

The colorless, sometimes granular, protoplasm is enclosed by a mem- 
brane, and some forms are surrounded by a transparent capsule. Not 
infrequently parts of the protoplasni appear less 
dense than the rest, as if from vacuolation, and a 
few observers have claimed to demonstrate in cer- 
tain forms a nuclear structure. But owing to their 
t _rt-^ifrtriv minuteness, studies of the structure of the proto- 

V \ f^"^ plasm of bacteria have thus far led to but meagre 
\ C ^-1 results. 

\. J Many of the bacteria, especially bacilli and 

^ spirilla, less frequently the cocci, have hair-like 

nu. 70.-TYPICAL FORMS proccsscs called tagella which are apparentlv or- 

OF Bacteria. Cocci, Ba- ./ ^ x-i c. 

ciLLi, and Spirilla. gaus of locomotlou (Fig. 71). These may be single 

or in tvifts ; may be at one or at both ends or over 
the general surface. Their number and distribution seem sometimes to 
be characteristic of special forms. 

Forms of Bacteria. — The various forms of bacteria may be grouped 
into three classes (Fig. 70). 

1. Spheroidal bacteria. — Cocci or micrococci (singular, coccus," micro- 
coccus). 

^ The term micro-organism includes all of these forms of minute and lowly plants. 
They are sometimes spoken of collectively as germs or microbes. 
'^Pronounced kok'-ns, phxYoX kok'-si. 







PLAXT PARASITES. 141 

2. Eod-liJce bacteria. — Bacilli (singular, bacillus). 

3. Spiral bacteria. — Spirilla (singular, spirillum). 

All straight bacteria which have one axis longer than the other are 
called bacilli, even though the form is oval rather than rod-like. The 
ends of bacilli may be square or 
rounded, and in stained preparations 
in some cases concave. 

While the cocci elongate a little 
in preparation for fission and in 
this condition present a slight ir- 
regularity in the length of their 
axes, and thus resemble bacilli, the 
complete observation of their life tig. ti.-bacilli with flagella. 

cycle rarely permits error in the de- 
termination of the primary group to which a given micro-organism 
belongs. 

Some bacteria present slight modifications of the fundamental form 
in certain phases of their growth and under various chemical and physi- 
cal conditions. Thus some of the cocci after division are slightly flat- 
tened on their contiguous sides — biscuit-shaped; certain bacilli may 
bulge slightly in the middle— Clostridium forms; others may be larger at 
one end than at the other — racket-shaped ; bacilli from the same culture 
may present considerable irregularities in breadth and size and length. 
The morphology may difl'er somewhat under different growth conditions. 
But these slight variations in form rarely give rise to serious difficulty in 
classification. 

AYhen the conditions of life are unfavorable bacteria may contain 
more deeply staining granules called metachromatic granules. These have 
been regarded by some as spores, but they ai)pear to be the results of 
cytoplasmic degeneration. The less degenerated portions retain the 
stain. 

Finally, when bacteria are placed under conditions unfavorable for 
the maintenance of their life processes, and when they are dead, they are 
often irregularly swollen and contorted or may 
undergo partial disintegration, giving rise to 
what are known as ^'involution forms. ^' 

#^ ypj While all bacteria are minute there is among 

"i /0j them considerable diversity in size, some being 

many times larger than others. ' 
FIG. 72. Bacteria avith Cap- When the bacteria are about to multiply by 

siLE. fission they elongate, a dividing septum forms, 

they become constricted at a right angle to the 
axis of elongation, and finally two independent organisms are produced. 
The multiplication of bacteria by fission may, when the conditions are 

^ P'or convenience of expression microscopists have agreed to let the letter ^ stand 
for tlie word micromillimetre, wiiich is one-thousandth part of a millimetre. This unit 
of measure, equal to about one-twenty -five thousandth of an inch, is often called a 




142 



PLANT PARASITES. 



favorable, occur so rapidly as to gi\e rise within a few hours to an enor- 
mous number of new individuals. 

In many cases, the new individuals thus developed fall apart in a 
form identical with that of the parent cell. In some species, on the 

other hand, the new -formed indi- 



•Vi 

/ 






Fig. 73.— Growth Aggregates of Bacteria. 



1. Diplococcus : 2, streptococcus 
4, diplobacillus ; 5, streptobacilli : 
forming chains. 



3, merismopedia ; 
6, curved bacilli 



vi duals are prone to cling together 
with greater or less tenacity, thus 
giving rise to growth aggregates 
which are more or less character- 
istic (Fig. 73). Thus among the 
cocci there are those in which a 
large part of the new individuals 
cling together in pairs. These 
forms are called diplococci. In 
others the pairs cling together in 
longer aggregates or chains. Such 
are called streptococci. 

A similar occurrence in the 
bacilli gives rise to diplobacilU and 
streptohaciM. Some of the spiral 
forms are due to the close junction 
end to end of oppositely curved 
segments. Certain long thread-like micro-organisms closely allied to the 
bacteria are called leptothrix. 

Certain cocci divide in two directions at right angles to each other, 
giving rise to four cocci clinging together and lying in the same plane. 
These are called merismopedia. 

Finally cocci may divide along three planes at right angles to each 
other, giving rise to cuboidal packets of eight germs or some multiple of 
this — such growth groups are called sarcina^ (Fig. 74). 

There is a family of filamentous or branching organisms which are 
often spoken of ^^polymorphous or higher bacteria, some of which may in- 
deed form a link between the bacteria and the 
lower fungi. Such filamentous forms are more or 
less distinctly segmented, and the segments may be 
enclosed in a common sheath. The modes of re- 
production and a certain specialization of function 
in different parts of the filaments which is fre- 
quently present indicate affiliations Avith higher 
fo]'ms. By this specialization of function is meant 
the attachment of the threads at one end to the 
substance on which they grow, and the formation 
at the free ends of structures which appear to be 
concerned in the reproduction. Several groups of these organisms have 
been named, but few of them have as yet been adequately studied. The 

^ Bacteria in masses embedded in and held together by a more or less abundant 
homogeneous material which they elaborate are called zooglaa. 




Fig. 74.~Sarcina. 

Showing growth aggregates 
in cuboidal 



PLANT PAEASITES. 143 

groups st) eptotlirix, dadotJirix, crenothrix, leptotlirix may be named. 
Among these tlie streptothrix is of most significance here, since i^atho- 
genic forms are known. The Streptothrix actinomi/ces, and closely related 
species, and the lesions which they induce, will be described later. 
There are many reasons for the belief that the forms called streptothrix 
and actinomyces are more closely related to the moulds than to the bac- 
teria, but the scope of this work does not permit the discussion of the 
subject, particularly difficult as it is on account of the confusion of 
terms and the lack of sufficient knowledge of the life history of the 
organisms involved (see Actinomyces, p. 199). 

Variations in Forms. — Their apparently simiDle structure and the lowly 
position which bacteria occupy in the scale of living things have given 
rise to the conjecture that marked changes in form within the limits of 
the primary grouj^s, or even changes from one primary group to another, 
may be brought about by alterations in environment, food, etc. In the 
early days of the exact study of bacteria this belief in pleomoriMsm in 
bacteria found readj^ currency. But the more exact study of separate 
forms, which the new technique has made possible, has led to the general 
acceptance of the view that variations do not occur except within com- 
parati^ely narrow limits, and that what we are accustomed to call species 
of bacteria maintain their morphological characteristics with tenacity 
under the most varied changes in enviromnent, even though these persist 
through the countless generations which may pass within the limits of a 
single experiment. The physiological characters of bacteria are, as we 
shall presently see, subject to wide and significant variation, but, so far 
as we can now see, monomo)p]nsm widely if not exclusively prevails. 

Spores. — Under a variety of conditions, the limitation of which are 
not very well understood, new bacteria are produced, and the species is 
peri^etuated, not by simple division, but by the de- 
velopment of spores. The most common mode of 
spore formation is called endogenous, A small, shin- 
ing mass makes its appearance within the proto- 
plasm from which it is formed, grows more and more 
distinct, and finally appears as a sharply defined 
spheroidal or oval, strongly refractile coloriess body ^'''' ' '';~cf spTres.^"'''' ' 
surrounded by a limiting membrane (Fig. 75), which The bodies of the baciiii 
can be separatelv stained and mav remain Avithin ^re stained with methy- 

,, T T ., "- ., ^, ir., , lene blue, the spores with 

the old ceil membrane or may free itself by rupture fuchsiu. 
of the latter. Endogenous S]3ore formation is com- 
mon in bacilli, rare in spirilla and in cocci. The spores appear to be 
surrounded by a dense envelope, and are, as a rule, much more resistant 
to deleterious agencies, such as heat, drying, chemicals, etc., than are 
the vegetative forms of the bacteria themselves. 

Vacuoles in bacteria are often mistaken for spores. Spores, when 
placed under favorable conditions in the i)resence of moisture and nutri- 
ment, swell, become less refractile, and develop into the usual vegetative 
form. The actual observation of this transformation is, in doubtful 






144 PLANT PARASITES. 

cases, the on! 3^ guarantee of the spore nature of these bodies. Another 
mode of sporulation — arthrogenous — has been described, but its nature is 
not well understood. 

Conditions of Life, Growth, and Multiplication. — The bacteria require 
for their nutrition carbon, hydrogen, oxygen, and nitrogen, and certain 
mineral salts. These thej^ can obtain from albuminoids and carbohy- 
drates. Free oxygen is necessarj^ for the growth and activities of some 
forms of bacteria and for others not. 

Those bacteria which require free oxygen are called aerobic. Those 
which do not grow in its i^resence are called anaerobic. But between 
these extremes there are forms which make shift to grow without oxygen 
under favorable conditions, though they make use of it when present ; 
others grow in its presence, though flourishing best in its absence : these 
are q.^\\q^ facultative aerobes or facultative anaerobes, in distinction from 
those first mentioned, which we call obligate aerobes or anaerobes. 

Nitrogen may be obtained by some bacteria from inorganic salts of 
ammonia, from nitrites and nitrates. Bacteria grow best as a rule in an 
organic food medium, especially soluble albuminous material which is 
neutral or slightly alkaline. Most of these materials are rendered avail- 
able as food by the action of enzymes— inverting, sugar-splitting, ]3roteo- 
lytic, etc. , often given off by the orga^nisms and acting upon the albu- 
minous materials. 

Bacteria are active only in the presence of moisture. When this and 
other conditions favoring their activity fail they do not necessarily die, 
but some forms may remain, either as spores or as fully developed organ- 
isms, for long iDcriods dry and inert, but capable of resuming their ac- 
tivity whenever they are again restored to favorable conditions. 

Some bacteria are and some are not very sensitive to changes of tem- 
perature. At a temperature below -f 5° C. they are incapable of marked 
activity or proliferation. At + 7° C. a slow growth has been observed 
in various species. Many forms may remain alive for long jDcriods frozen 
in ice, while some are not killed by a temj)erature of —111° C. As the 
temx^erature is raised their activities increase up to a certain point. It 
may be said in general that they are most active at about the temper- 
ature of the body, although species differ considerably in this respect. 
In fluids many bacteria are killed by a prolonged exposure to a temi^er- 
ature of from 60° to 70° 0. or even less. On the other hand, certain 
species grow at a temi)erature of from 60° to 75^ C. Such are called 
tJiermophiUc bacteria. When dry they resist much higher temperature 
than when moist. All known bacteria, save a fe^\^ ^ery invulnerable 
spore-forming species, are killed by prolonged exposure in the presence 
of moisture to a temperature of 100° C. The spores are, as a rule, more 
resistant to high temperatures than the bacteria themselves, some having 
been exposed, dry, to a temperature of 110° C. without destruction of 
life. Fluids containing the spores of bacteria which resist very high tem- 
peratures may be sterilized by boiling for a short time, then being allowed 
to stand at ordinary temperatures for several hours, and then again boil- 



PLANT PAEASITES. 145 

iug ; this process being repeated several times. lu this way, although 
the spores themselves are not killed by the heat, the bacteria into which, 
if the conditions be favorable, they develop during the intervals are 
killed, so that finally the medium is entirely freed from both living- 
spores and adult bacteria. 

Strong light is in general inimical to the life and growth of bacteria, 
and by direct sunlight many forms are readily killed. 

Motility. — Some bacteria are callable of performing rapid movements, 
others are not ; and the same form may be at one time motile and at 
another immotile, depending upon external conditions. Movement is 
largely confined to the rod-like and spiral forms, but has been observed 
in the spheroidal. 

It has been shown that certain of the motile bacteria, when suspended 
in fluids, are attracted toward, or repelled from, dissolved chemical sub- 
stances. This is called cJiemotaxis (see p. Ill), and it is termed positive 
or negative according as the organisms are attracted or repelled. 

Germicides. — Certain chemical agents, when brought into contact with 
bacteria, greatly reduce their activities or destroy their life altogether ; 
but different species differ greatly in their capacity of resistance to 
these agents. The spores of certain bacteria are exceedingly resistant, 
much more so than the bacteria themsehes, to the action of disinfecting 
agents. Among the chemical substances commonly used as disinfectants 
may be mentioned formalin, carbolic acid, and especially solutions of 
corrosive sublimate, which is very inunical to the life of most bacteria 
and their spores, even in extremely dilute solutions. 

The Distribution and Role of Bacteria in Nature ; Metabolism, etc, — 
The bacteria play a very imi^ortant role in nature in virtue of their power 
of feeding upon and decomi)osing dead organic material. A part of the 
new chemical compounds which are thus formed may be used by the bac- 
teria for the purposes of their own nutrition and growth, while the rest 
are set free to serve, sooner or later, as food for other forms of plants or 
animals. In the decompositions which are brought about in nature by 
the bacteria those compounds of nitrogen and carbon dioxide are set free 
which are essential for the nutrition of the higher plants. 

Without the activities of bacteria, life could not be long maintained 
upon the earth, since the necessary carbon, hydrogen, oxj^gen, and nitro- 
gen would soon be permanently locked up in unavailable form in organ- 
ized material. 

Through the action of the various nitrifying bacteria in the soil, am- 
inonia is decom]DOsed with the formation of water and nitrous acid ; nitrous 
is converted into nitric acid. The so-called denitrifying bacteria reduce 
nitrates to ammonia and to nitrites. In these ways, among others, water 
percolating through the soil may be freed from objectionable organic 
comxDounds. 

A large number of complex chemical substances are elaborated dur- 
ing the growth of bacteria, their nature A^arying with the species of bac- 
teria and the composition of their nutrient material. Some of the 
10 



146 PLANT PARASITES. 

chemical compounds set free by the growing bacteria are bad-smelling 
or aromatic ; some are inert and harmless substances ; some are powerful 
poisons, and may, when they have accumulated in the fluids where they 
grow, inhibit activity and growth or even destroy the bacteria which 
have produced them. 

Fermentations and i)utref actions are due to the activities of micro- 
organisms, some to bacteria, some to yeasts, some to moulds. Putrefac- 
tion is a form of fermentation in which nitrogenous compounds are 
decomposed by micro-organisms setting free, especially in the absence of 
oxygen, bad-smelling substances. 

Bacteria which induce fermentation are called zymogenic — and each 
species induces fermentation of a particular character in the presence of 
a special substance, as glucose, or members of a certain class of substances 
such as carbohydrates. Some of these fermentations are important in the 
arts ; some are concerned in the changes which food products undergo 
under natural or artificial conditions, such as the development of 
koumyss from milk and the common butyric, lactic, alcoholic, and other 
fermentations. 

The chemical changes which are induced by micro-organisms in the 
process of fermentation are extremely comi^lex and little understood. 

Bacteria may develop in their metabolic activities soluble ferments 
or enzymes of various kinds resembling diastase, pepsin, trypsin, rennet, 
etc. These may remain in the bacterial cell or may be diffused into the 
surrounding media. 

Many bacteria form pigments as they grow {chromogenic bacteria). 
This pigment may be developed in or ui)on the germs themselves or may 
be diffused through the surrounding media and may be developed only 
in the i)resence of light, oxygen, etc. Gas-producing bacteria are called 
((erogenic. Certain species when growing in masses emit a phosphor- 
escent light — photogenic bacteria. 

Certain of the basic chemical compounds resembling the vegetable 
alkaloids, which are formed by the action of bacteria in organic matter, 
are called ptomains. ' The chemical substances produced by certain forms 
of bacteria are of practical importance because they induce deleterious 
effects in many of the infectious diseases ; these are called toxins. Com- 
plex proteid bodies may be produced during the growth of bacteria; 
these may be in part set free, in x)art assimilated in the bacterial cell 
protoplasm. These proteid bodies belong in part to the albumins, in 
part to the albumoses, while some of them resemble the peptons. Many 
of them seem to be most potent factors in the induction of the phe- 
nomena and lesions of the infectious diseases. The poisonous albumi- 
nous substances produced in the body by the growth of certain disease- 
producing bacteria are called toxalbumins. These may also be produced 
in culture media. 

Bacteria are widely distributed in the air, in water, and in the super- 

1 Leucomains are basic products produced in the tissues of living animals by cell 
metabolism. 



PLANT PARASITES. 147 

ficial layers of the soil, where they may be present in enormous numbers. 
They are especially abundant among the habitations of man, or wherever 
under favorable conditions of moisture and temperature animal or vege- 
table substances are undergoing decay. They cling tenaciously to moist 
surfaces, but when dried, and esiDCcially when dried uj^on comminuted 
material, they may float in the air as dust. In quiet air they gradually 
settle with other forms of dust on to horizontal surfaces, and thus in 
closed, still rooms the bacteria -laden air may in a few hours almost wholly 
free itself of its living contaminations by a process analogous to sedimen- 
tation in water. 

This widespread transportation of bacteria as dust by moving air, and 
the spontaneous cleansing of the latter by the settlement of the germs, are 
important factors in the sanitary problems which the complex conditions 
of modern life present. 

While bacteria may live for long periods in the dried state in dust 
they do not in this condition multiply. But the upper three or four feet 
of the soil forms the great abiding, and when moist the breeding, place 
of the myriads of germs which are concerned in the salutary work of 
food preparation for higher plants. Large numbers of mould spores are 
frequently mingled with the bacteria in dust and soil. 

Surface waters almost always contain bacteria, which may have en- 
tered by aerial dust or from the wash of adjacent soil or from direct 
human or animal contamination. Many bacteria find in water favorable 
conditions of life and flourish on what to other forms would be but scanty 
iRitriment^ Many pathogenic bacteria may remain alive for considerable 
periods in water, but they do not usually thrive there. 

The water which in many places lies in hollows of the rocks, bathing 
the deeper layers of the soil or gathered in caverns and recesses beneath, 
is called ground tcater. This under favorable conditions is almost wholly 
free from micro-organisms, these, through the complex process of filtra- 
tion, germ metabolism, etc. , which go on in the upper soil layers, having, 
together with inorganic contaminations, been largely retained or trans- 
formed as the surface water has slowly sought the lower levels. 

The Relationship of Bacteria to Other Living Beings. — So far as we 
know, with few exceptions the bacteria whose natural habitat is the soil 
or air or water are not under usual conditions harmful to man. On the 
other hand, it is germs from the bodies of men or animals who are the 
victims of infectious disease, gaining access in one way or another to 
these great reservoirs and sources of distribution, which occasionally ren- 
der the bacterial flora of soil, and air, and water of direct personal sig- 
nificance to man. 

It will be seen from what has been said about bacteria and their vari- 
ous modes of life that some live in or upon and at the expense of other 
living beings — ^the hosts — these are parasites. Others T\'hich live and 
grow apart from a living host are called saprophytes. In either class there 
are forms which, through the capacity of adapting themselves to their 
environment, can maintain at one time a parasitic, at another a sapro- 



148 PLANT PARASITES. 

phytic life. Such germs are called respectively /acw^Mu^e parasites or 
facultative saprophytes. Those, on the other hand, whose life is strictly 
limited to the parasitic or saprophytic condition are called oUigatory 
parasites or saprophytes. 

^ot all the bacteria which live in or upon the bodies of men and 
animals are in the stricter sense parasites. The terms messmates and 
commensals have been applied to such organisms as simply live with, but 
do not necessarily derive nutriment from, the host. 

In some cases parasitic life on the ijart of the micro-organism may 
contribute to the welfare of the host. This is the case in some bacteria 
which live upon the roots of certain leguminous plants, and to whose 
nutrition they contribute by rendering atmospheric nitrogen directly 
available for the host. This condition of life is called symbiosis. 

Species and Varieties. — As has already been indicated, the morpho- 
logical characters of bacteria are so little subject to permanent variation 
under the widest diversity in the conditions to which they are subject 
that we are justified in the belief in fixed species. But so susceptible to 
external condition are the functional activities of many species that not 
only is the occurrence of what may be called varieties within specific 
limits frequent under natural conditions, but more or less permanent 
variations may be experimentally produced. 

Almost all of the functional activities of bacteria upon which we rely 
as descriptive characters may be experimentally altered ; thus the color- 
producing capacity may be diminished, the iDcptoniziug and fermentatiA e 
activities lowered, the pathogenic powers reduced or exalted, and even 
the capacity for spore formation may be abolished. 

These more or less permanent modifications of function in bacteria 
may be induced by artificial cultivation under adverse conditions of tem- 
perature and nutrition, by the presence of deleterious chemical agents, 
antiseptics, etc., or by association with the body cells and juices in sus- 
ceptible or insusceptible animals. 

CLASSIFICATION OF BACTERIA. 

The beginning of the systematic study of bacteria by exact and re- 
liable methods is of such recent date, they are so minute, and our present 
optical apparatus reveals so few differential morphological characters 
beyond the limits of the three primary classes already mentioned, and so 
few withal of the many existing forms have as yet been studied, that a 
satisfactory classification or nomenclature of the bacteria is not yet pos- 
sible. 

Outside of the limit of the primary classes above described and based 
upon the shape, we are obliged to use for the purposes of identification 
and description the results of physiological activities which the special 
forms of bacteria display when placed under diverse and usually entirely 
artificial conditions of food, temperature, and general environment. It 
is evident from this condition of affairs that what in our attempts at 



PLANT PARASITES. 149 

classifications we are wont to call genera and species, are not such in the 
strict sense in which these terms are used in other domains of biology. 
That which corresponds to the generic name in the more exact vocab- 
ularies is in ours usually the growth form which indicates the primary 
class to which the germ belongs, as coccus, bacillus, or spirillum, or some 
growth modification of this, as diplococcus, streptococcus, streptobacillus, 
and the like. To this is usually appended a more or less distinctive 
specific name, which ordinarily indicates some noteworthy physiological 
capacity of the germ, such as its peptonizing power, the pigment which 
it elaborates, some prominent chemical reaction which it initiates, some 
marked effect upon an artificial culture medium, its disease-producing 
power in men or animals, or some fact about its habitat, or the situation 
in which it was found. All of these and other heterogeneous character- 
istics, largely functional, which may be developed under natural or arti- 
ficial conditions, constitute data in the life history of germs upon which 
the classification and nomenclature of bacteria are at present based. 

As examples of names of bacteria thus derived may be cited Micro- 
coccus lutcus, Diplococcus lanceolatus, Scvrcina vcntriculi, Bacillus acidi lac- 
tici, Spirillum ckolerce Asiaticce. 

I*^otwithstanding the value of this principle of grouping and nomen- 
clature, its inadequacy even for temporary use is becoming painfully 
evident as research proceeds, partly because of the large variations to 
which physiological acCvities are liable, and partly because we cannot 
sharply distinguish between races, varieties, and species. 

It is not yet possible to say whether it will ever be practicable in this 
limited field of lowly life to draw such exact distinctions between genera 
and species as is iDOSsible among higher organisms. 

Methods of Morphological Study of Bacteria. 

The simplest mode of studying bacteria is to examine them either in the fluids in 
which the}^ grow or in one-half-per-cent salt solution. For the study of many of the 
phenomena of life this method is important. 

This may be accomplished by the examination of a thin layer of the fluid under a 
cover slip, in the usual way; or a small drop may be placed on the cover slip and this 
inverted on a hollow slide so that the observation is made in the hanging drop. A 
streak of vaselin painted around the edge of the cover will prevent evaporation of the 
fluid. 

Staining. — By far the most important aid in the morphological study of the bac- 
teria is derived from the use of staining agents. Most of the bacteria are stained more 
or less readily by one or more of the basic anilin dyes. The ease with M^hich they are 
colored varies considerably in different species and with the different dyes. The tissue 
elements, and a variety of other materials with which the bacteria may be associated, 
also stain more or less readily at the same time; but most of these part with their color 
more readily than do the bacteria on being treated with alcohol or dilute acids. It is 
thus possible to obtain a differentiation in color between bacteria and other structures. 
The bacteria, moreover, differ among themselves in respect to the tenacity with which 
they hold their stain in the presence of decolorizing agents, and upon this fact is based 
one of the important methods of distinguishing between different species. 

Among the anilin dyes more commonly employed for bacteria staining may be 
mentioned fuchsin and methylene blue. A saturated alcoholic solution of these dyes 



150 PLANT PARASITES. 

should be kept in tightly stoppered bottles, and from these the more dilute solutions 
required foi staining may be prepared. For ordinary purposes one part of alcoholic 
solution of fuchsin or methylene blue, added to twenty parts of water, will give a 
staining solution of suitable strength. 

Special stains and modes of staining, such as are necessary for some forms of bac- 
teria — the tubercle bacillus, for example — will be described under the appropriate head- 
ings. 

To Stain Bacteria in Fluids. — A small drop of the fluid is placed on a clean cover 
glass, spread a little with a needle, and dried by gentle heat. The cover glass is now 
held with the forceps, specimen side up, and passed moderately rapidly three times 
through the flame of an alcohol lamp or Buusen burner. The material on the cover 
should not be burned. This heating not only fixes the contents of the fluid firmly on 
to the glass so that it will not easily soak off, but renders insoluble any albuminous 
materials which may be mixed with the bacteria, and which might otherwise interfere 
with subsequent examinations by forming granular precipitates. 

A drop of the aqueous staining fluid is now put on to the dried specimen on the 
cover glass, and if this be held in the forceps and tilted slightly up and down a few 
times so as to bring fresh portions of the staining fluid into contact with the bacteria, 
the staining will usually be completed in two or three minutes. The stain is now 
washed off with a jet of water from the wash bottle, and the specimen is either mounted 
in a drop of water for temporary study, or the washing water is drained off and, after 
drying in the air, it is mounted directly in balsam. It is well to use balsam which has 
been softened, when this is necessary, with oil of cedar or xylol rather than with chloro- 
form, since this is apt to decolorize the bacteria. Solid cultures of bacteria should be 
mixed with a little water and spread on the cover glass before dr3ing and staining. 

Gram's method (see below) is often useful and in some cases almost indispensable for 
the differential staining of bacteria. ' 

To Stain Bacteria in Tissues. — The tissues should be well hardened in alcohol. 
Thin sections are placed in the above-described aqueous coloring solutions, where they 
may remain from five to fifteen minutes. In some cases a much longer staining is nec- 
essary. Gentle warming (40° to 50° C.) will hasten the staining. The entire tissue as 
well as the bacteria is in this way deeply colored. The sections are rinsed with distilled 
water and then placed in alcohol. This, with varying degrees of rapidity with differ- 
ent stains and tissues, gradually extracts the color from the tissue, most slowly from 
the nuclei. The time required and the exact degree of decolorization to be sought for 
must be learned by experience in different cases. Sometimes five, sometimes thirty 
minutes are required, sometimes only a few seconds. It is often necessary, and the 
decolorizing of the tissue is thereby hastened, to add a few drops of acetic acid to the 
alcohol. When acetic acid is used it should be finally thoroughly washed out by alco- 
hol. The specimens are now cleared up by oil of origanum and mounted in balsam. 
In specimens prepared in the above way, the nuclei of cells usually retain to some ex- 
tent a color similar to that of the bacteria, but their size and shape serve for the differ- 
entiation. 

Gram's Method. — This is a much more generally useful method of staining bacteria 
in the tissues than that just given, although not in all cases applicable. The sections 
are stained for from two to four minutes in anilin-gentian-molet solution, prepared by 
adding 1 c.c. anilin oil to 20 c.c. distilled water, shaking thoroughly, and filtering 
off the excess of anilin oil through a moistened paper filter. To the clear filtrate satu- 
rated alcoholic solution of gentian violet is added in the proportion of about 1 of the 
dye to 10 of the anilin solution. 

From the staining solution the sections are transferred to a solution of iodin in 
potassium iodid and water (I 1.0— KI 2.0— H2O 300.0), remaining from one to three 
minutes, when they are transferred to strong alcohol; this should be changed two or 
three times so as to dehydrate the specimen, which at the same time will lose much of 
its color. The section is cleared in oil of origanum to which a little eosin has been 

^ For the methods of staining spores see special works on bacteriology. 



PLANT PARASITES. 151 

added, and mounted in balsam. In specimens prepared in this way the bacteria and 
some of the nuclei are violet, the remainder of the tissue is red. 

In this as in other methods of staining bacteria in tissue the sections are liable to 
shrivel and curl. This may in many cases be avoided by fixing the sections on to the 
cover slip with albumen fixative (see page 52) before the staining begins, carrying 
cover glass as well as section through the subsequent processes. Since some bacteria 
are decolorized by Gram's method it is not applicable to the staining of all organisms in 
tissues. It is often a valuable aid in the differentiation and identification of species with 
similar morphology — and in some instances, as in the staining of gonorrhoeal pus, has an 
especial diagnostic value (see page 194). 

Weigerfs Modification of Gram's Method. — The sections are laid for half an hour in 
the anilin gentian- violet solution prepared as above, then rinsed off in three-quarter- 
per-cent salt solution, and spread on a slide. They are now dried with blotting-paper 
and covered for two minutes with the iodin solution. The iodin solution is now washed 
off in the water, the section dried with blotting-paper, and decolorized with anilin oil 
or a mixture of 2 parts of anilin oil and 1 part of xylol, several times renewed. Finally 
the sections are cleared in xylol and mounted in balsam. 

In many cases it is well to accomplish a double staining by a preliminary contrast 
stain. Thus, before the use of Weigert's modification of Gram's stain the sections may 
be put for half an hour in a solution of picro-carmin, then rinsed in water and stained 
as above. By this modification of Gram's method fibrin is deeply stained. 

Loffler's alkaline-methylene-bliie solution is a very valuable and powerful stain for 
bacteria, either in fluids or in tissues. 

It consists of — 

Saturated alcoholic solution of methylene blue, . . .30 parts. 
Aqueous solution of caustic potash 1 : 10,000, . . . 100 

For staining bacteria in tissues the stain is allowed to act for a few minutes. The 
.section is then put for a few seconds in one-half-per-cent acetic acid, then rinsed in 
water, and the superfluous color removed from the tissue by repeated rinsing in alco- 
hol, which at the same time dehydrates it. Then it is cleared with oil of cedar and 
mounted in balsam. Care should be taken not to remove too much color with the 
alcohol. 

It should always be borne in mind in staining the bacteria that great exactness is 
not usually necessary either in the strength of the coloring solutions or in the time of 
exposure of the bacteria to them. We are seeking for certain effects — namely, the 
staining of the germs — and this depends not only upon the quality and strength of the 
dye, the time of exposure, etc., but also upon the nature of the bacterial species and its 
conditions at the time the staining is undertaken. Thus it not infrequently happens 
that bacteria which will stain readily and deeply with a given solution when they are 
in a condition of active growth, may be scarcely at all colored if they have been dead 
or inactive for a long time, although their outward shape appears to be unchanged. 
So it should be remembered that, while there is little difficulty in most cases in staining 
the bacteria, the operation is not one of mere routine, but requires intelligent attention 
to the particular conditions of the species in hand. 

For the recognition and study of bacteria the best optical apparatus is requisite. 
An homogeneous immersion lens (at least one-twelfth) and the Abbe condenser are in- 
dispensable for ordinary work. 

Artificial Cultivation of Bacteria. 

For the complete investigation of the different forms of bacteria, particularly in 
their relations to disease, we must isolate them so as to be able to study their life his- 
tory and the effects of their inoculation into healthy animals. It has long been known 
that bacteria could be cultivated in a variety of artificial, so-called "nutrient media" or 
soils. Fluids were formerly used for this purpose, but it is very difficult to separate 
single species in fluids. Robert Koch introduced, a few years ago, a technical improve- 



152 



PLANT PARASITES. 



ment of great value in the use of solid media for the eultivation of bacteria. They 
usually grow within or upon the surface of the solid nutrient media in sharply circum- 
scribed masses, called colonies, and diiferent species may grow side by side in the same 




Fig. 76.— a Pktri gelatin Plate Culture of Bacteria from Milk. 
In one plate there are few colonies showing difference in size and character. In the other the colonies 
are much more abundant. 



receptacle for considerable periods without in the slightest degree interfering with one 
another or tending to mix. The mode of growth and general appearances of the pro- 
liferating bacterial masses on the solid medium often present very characteristic differ- 
ences between different forms, and thus not only furnish valuable means of identifying 
species, but render possible an early detection of contamination from chance admixture 
of species. A given species of bacteria may be cultivated through a series of genera- 
tions by transferring, with proper precautions, a minute portion from a growing colon}' 
to a fresh surface of sterilized soil. After cultivation tiirough several generations the 

species may be presumed, and by micro- 
scopical examinations proved, to be en- 
tirely pure, and the effects, if any, pro- 
duced by its inoculation into healthy 
animals, to be due to it alone. 

The Culture Substances. — There 
are many culture media, some of which 
are best suited for one, some for another 
species of bacteria. Those most com- 
monly used are meat broth (bouillon), 
broth rendered solid by gelatin or agar- 
agar (called " nutrient gelatin " or " nu- 
trient agar"), boiled potatoes, milk, 
coagulated blood serum, pleuritic " chest 
serum," or other transudates into the 
serous cavities. Glucose is often added 
to the media for special purposes, and 
the incorporation of litmus serves to 
mark the formation of acids or alkalies 
as the result of bacterial metabolism. 
Various special forms of artificial media 
are also employed. (For the details of the methods of preparing culture media con- 
sult special works on bacteriology, such as Ahhotfs " Principles of Bacteriology " or 
Park's "Bacteriology in Medicine and Surgery.") These various forms of media arc 




Fig. 



-Colonies in Gelatin Plate Culture. 



This cut shows a small portion of the culture, Fig. 
76, magnified. Some of the colonies are very small, 
others of a different species are large and spreading. 



PLANT PARASITES. 



153 



placed in small quantities in test-tubes plugged with cotton (Fig. 78) and carefully 
sterilized by heat. 

The Study of Cultures. — Let us see how the nutrient media are used in study- 
ing the bacteria. 

In the first place, it is necessary to get from the various mixtures of several species, 
as they are apt to occur in nature or in diseased parts, single species growing by them- 






FiG. 78. Fig. 79. 

Fig. 78.— Pure Culture of Bacteria on Nutrient Agar in Sterilized Tubes. 

Showing at the left a smooth, at the right a wrinkled growth upon the surface. 

Fig. 79.— a Culture of Bacteria on Potato. 



selves, so that their life history and characters may be studied in detail. To show by 
an example how this is done, we will suppose that we have a sample of milk containing 
bacteria, and wish to learn how many there are and of what species, and to get them 
into separate receptacles for study. We melt the nutrient gelatin or agar in one of 
the test tubes, which we know to contain no living bacteria — because we have steril- 
ized both the tube and its contents l)y heat — and add to it a measured volume, usually 



154 



PLANT PARASITES. 



0.01 c.c, of the milk, and mix them by gentle shaking; we now take a shallow covered 
glass dish called a Petri plate (see Fig. 76), wliich has been sterilized by heat, lay it 
upon a cold surface, and pour out the mixture of milk and nutrient gelatin in a thin 
layer upon it. "When the gelatin solidifies, the invisible germs which the milk contained 
are caught and held in position by it, and if the whole be now set away in a sufficiently 
warm place the living bacteria will presently commence to grow. 

After a few hours or days, from each one of the single living bacteria scattered 
through the gelatin so many new germs may have developed that they form a mass, 
called a colony, large enough to be visible to the naked eye. As different species grow 
in different ways, some giving rise to colonies of one shape or outline, some to another ; 
some forming colored colonies, some fluidifying the gelatin, some growing much more 
rapidly than others (see Fig. 77), we can usually recognize the difference in species 
either with the naked eye or under the microscope, and with a fine, sterilized platinum 
needle can pick out portions of the different colonies and transfer them to the tubes of 
nutrient media of one kind or another which we have prepared, and study their growth 
there in the form of pure cultures. 

The transfer of the germs to the tubes is made by plunging the needle which has 
touched the plate colonies down into the gelatin or agar, or drawing it over the surface 

of the potato or agar (Figs. 78, 79, and 80). 
This is called inoculating the culture media. 

Not infrequently it is necessary to use the 
agar culture medium instead of gelatin for 
plate cultures, because many disease-producing 
forms of germs do not grow at a temperature 
below that of the body, at which gelatin fluid- 
ities. 

In many cases, especially in agar plate 
cultures, the material to be studied is spread 
in very thin streaks, with a sterilized platinum 
needle, over the surface of the already cooled 
nutrient film, the colonies developing along the 
surface streaks (see Fig. 81). 

Anaerobic germs may be cultivated in an 
atmosphere of liydrogen, the air in the closed 
culture receptacles being replaced by this gas. 
Or the oxygen may be removed from this con- 
fined portion of air in contact with the cul- 
tures by chemical means. A description of the 
various simple and complex devices for anae- 
robic cultivations falls beyond the scope of 
this work. 

The most scrupulous care is required in 
sterilizing the nutrient media and the utensils 
and instruments used, and the greatest caution 
should be exercised, in transferring the bac- 
teria from one receptacle to another, to pre- 
vent contamination. A large experience in 
this sort of manipulation is necessary before 
reliable results can be obtained in original in- 
vestigation, since the slightest error or care- 
lessness in handling, or failure to observe the occurrence of contamination, is liable 
entirely to vitiate the results of long series of experiments. It is only by an extended 
preliminary training in the cultivation of some of the more characteristic and easily 
recognizable forms, under a variety of conditions, in a perfectly pure state, through a 
series of generations, that one can be assured of his capacity to carry on researches in 
this most difficult and intricate field. 

It is wiser for one purposing to carry on bacterial researches to gain a practical 




Fig. 80.— a Tube of Solid Transparent 
Nutrient Gelatin. 

Showing growth of bacteria with formation 
of gas along the line of inoculation by a nee- 
dle plunged into the solid gelatin and with- 
drawn. The bacterial masses are held fast 
where they grow, and the gas bubbles cannot 
escape through the solid media. 



PLANT PARASITES. 



155 



acquaintance with methods and apparatus in a well-appointed laboratory, than to make 
■be attempt to work out the methods from books. 

The methods of inoculation of animals with pure cultures, and the precautions to 




Fig. 81.— Petri's Agar Plate Culture of Bacteria from the Mouth. 

Made by streaking the surface of sterilized nutrient agar— previously poured into the shallow dish and 
cooled— with scrapings from the mouth, and allowing to stand in a warm place for forty-eight hours. The 
lighter spots are the " colonies " or masses of germs of various forms which have grown from the invisible 
germs of the mouth. 

be observed, as Avell as a description of the various forms of apparatus made use of in 
practical bacteriology, must be sought in more extended treatises on this subject. 

Collection of Material for Bacterial Cultures. 

Material obtained from the human body which is to be subjected to bacterial ex- 
amination should be collected with every precaution against accidental contamination. 



^?tf.^^''P ' ^--:^Wn^'^^ 



Fig. 82.— Sterilized Cotton Swab in a Sterilized Tube for Collecting Fluids Containing Bac- 
teria. 

A convenient mode of collection and transportation of small quantities of fluid or 
semi-fluid material, such as exudates, discharges, etc., for purposes of bacterial examina- 




156 PLANT PARASITES. 

tion is to twist a small wad of absorbent cotton on to the end of an iron or steel wire 
about five inches long, put this, swab end foremost, into the tube (Fig. 82), plug the 
mouth with cotton, and sterilize the whole in a dry oven for an hour at 1(50" C. 

Several of these cotton swabs may be prepared at once and kept on hand. The 
swab, carefully removed and saturated with the material to be examined, is at once re- 
turned to the tube; this is plugged, and may be thus safely transported. ^ 



II. Yeasts. 

These micro-organisms — mostly saprophytes — consist of oyal or 
spheroidal cells with grannlar protoplasm and a thin membrane. They 
multiply by sprouts or buds from the parent cell (Fig. 
83). The new individuals may separate from the old, 
or may cling to them so that chain -like combinations 
may occur. They sometimes form endogenous spores, 
known as ascospores. Some species develop bright 

„„ , „ colors in their growth. 

Fig. 83.— Yeast— Sac- ^^ ° ^ ^ . i • i 

charomyces. There are many forms of yeasts which are concerned 

in various phases of fermentation. Some of these, al- 
coholic fermentation for example, are of great economic importance." 
Certain forms of yeasts flourish in the stomach during digestive disorders 
and in the bladder in diabetes, without the incitement of lesions. Sev- 
eral forms of yeast have been proven to be pathogenic in lower animals 
and in man. In 1894 Gilchrist ^ reported a case of blastomycetic derma- 
titis in man. Since that time other cases have been observed. " 



III. Moulds. 

The moulds are considerably more complex in structure than either 
the bacteria or the yeasts. Some of the forms are very common and uni- 
versally known. In general, it may be said that the moulds consist of 
a series of delicate, translucent, branching jointed threads — mycelium — 
usually giving rise to hyphce from which, either directly or in more com- 
plex form through the intervention of a special structure, the sporangium, 
the spores are developed (Fig. 84). The moulds which are apt to occur 
in the human body may be of the former more simple, or of the latter, 
more complex type. ° Among the simpler forms of moulds which occur 
in the body may be mentioned the Achorion Schonleinii, Microsporon 

^ For further suggestions for the collection and examination of specimens for micro- 
organisms, and for references to studies on the bacteria of the human body, see p. 260. 

"For a consideration of the relationship of micro-organisms to various forms of fer- 
mentation, with bibliography, consult Jorgensoii, "Micro-organisms and Fermentation," 
Eng. translation, 1900. 

2 Gilchrist, Johns Hopkins' Hospital Reports, vol. i., p. 269. 

'^ For a resume of the subject of pathogenic blastomycetes with experiments and 
bibliography, see Foulerton, Journal of Pathology and Bacteriology, vol. vi., p. 37, 

^See Renon, " Etude sur I'aspergillose chez les animaux et chez I'homme," Paris, 
1897; also Leopold and Levi, Gaz. des Hopitaux, June 26th, 1897, Bibl. ; also Pierson and 
Bavenel, University Med. Mag.. August, 1900; sXso Sayer, "Pneumonom^^kosis asperdl- 
lina," Jena, 1900. 



PLANT PARASITES. 



15- 




Fig. 84.— Aspergillus Glaucus. 

Showing mycelium, from which arise the spore- 
bearing structures, the sporangia home upon the hy- 
pha?. 



furfur, Trichophytou tonsurans. There is a close morphological resem- 
blance between these forms. 

Achorion Sclwnlemii, the favus fungus, is formed of a much -branching 
mycelium from which the spores are directly developed (Fig. 85). It 
grows readily on artificial cul- 
ture media, such as nutrient agar 
and gelatin, at the temperature 
of the bodj , This fungus is most 
apt to grow ux3on the hairy part 
of the head, where it forms small 
surface crusts and grows into the 
shafts and root sheaths of the 
hair, exciting inflammation in the 
adjacent tissue. Trichophyton ton- 
surans develops in the form of a 
moderately branching mycelium, 
forming comparatively few spores. 
It grows in the skin, either about 
or apart from the hairs, or in the 
nails, inducing the lesions of vari- 
ous phases of heriDCS, which differ 
considerably, depending ui)on the 
particular structures involved. 
At body temperature it grows readily on artificial culture media, differ- 
ing markedly in appearance from Achorion. 

Microspor on furfur, the mould fungus causing pityriasis versicolor, is 
more prone than the Achorion to the development of many spores, but 
otherwise considerably resembles it morphologicallj^ It has not yet been 
cultivated on artificial media. By its infiltration of the epidermis, espe- 
cially of the body and upper extremities, 
it causes larger and smaller yellowish or 
brownish patches. 

The more complex types of moulds are 
only occasional dwellers in the human 
body and appear to be but rarely the 
cause of disease, passing, rather, a sapro- 
phytic existence on dead material in parts 
of the body which are in communication 
with the air. Thus they may be found 
growing on accumulations in the external 
auditory canal, in dead tissue in the 
lungs, on walls of cavities, dila;ted bron- 
chi, etc. Many cases have been reported, 
however, in which the moulds, especially 
aspergillus, have been the apparent excitants of serious lesions in men 
and animals. 

A lowly form of micro-organism frequently found growing in the 




Fig. 85. 



-Achorion Schonleinii- 
From a culture. 



-Fatus. 



158 PLANT PARASITES. 

mouth and fauces aud oesophagus of children, in the form of a whitish 
pellicle — aphthae — is the so-called Oidiiim albicans, which consists of 
branching, jointed threads and spores which penetrate between the epi- 
thelial cells. This fungus may assume considerable importance, when 
in very feeble children it blocks the oesophagus, or when, as is rarely the 
case, from the surface of ulcers it penetrates the blood-vessels and gives 
rise to visceral metastasis. The exact relationship of this fungus to the 
moulds is not yet very clear. It is often grouped with the yeasts. ' 

Methods of Studying Yeasts and Moulds. 

The 3^east organisms are in general stained and cultivated by the same methods as 
those used in studying the bacteria. By treating unstained sections of tissue contain- 
ing them with sohition of caustic potash the organisms may often be readily demon- 
strated. 

The moulds may be simply teased and studied in glycerin or in glycerin and water. 
They may be stained with alkaline-methylene blue solution (Loffler's solution, see page 
151). When spores have formed in considerable numbers on the more complex forms 
of moulds these are not easily wetted by the usual staining fluids, because the air clings 
so closely among the spore masses. In a mixture of four parts of alcohol and one of 
aqueous solution of ammonia they are instantly wetted, and may then, with or without 
staining, be teased and mounted in glycerin. In studying the fungus masses in the 
above -described skin diseases it is well, when crust-like masses are to be teased apart, 
to allow them first to soak for a few moments in a five-per-cent solution of caustic 
potash. In this solution they may be studied, or they may be teased and mounted in 
glycerin for preservation. Most of the more common moulds are readily grown on the 
ordinary culture media. 

1 For resume and bibliography of relationship of yeasts and moulds to human dis- 
eases consult Bicker, Lubarscli, and Ostertag's "Ergebnisse der allg. Aetiologie der 
Menschen- u. Thierkrankheiten," Abth. i., 1896, p. 892. See also Hektoen, Journal of 
Experimental Medicine, •vol. v., p. 77, 1900. 



CHAPTER VII. 

THE RELATIONS OF MICRO-ORGANISMS TO DISEASE- 
INFECTION AND IMMUNITY. 

The Occurrence of Bacteria and Other Micro-organisms in 
the Body : its Protective Mechanism. 

Bacteria are invariably present in greater or less numbers in the 
mouth, nose, upper air passages, gastro- intestinal and genito- urinary 
tracts of men and animals. ' Into these x)laces they are more or less con- 
stantly brought by the resx)ired air,'' by food and drink, and in other 
ways. But common and often abundant as are these germs upon the 
external and internal surfaces of the body, they do not often pass through 
the healthy mucous or cutaneous surfaces, so that under normal condi- 
tions the tissues, the viscera, and the circulating fluids are germ-free. ^ 

Except for certain pathogenic forms which may, under unsanitary 
conditions, have been set free and transported from men or animals 
suffering from infectious disease, the bacteria upon the cutaneous or 
mucous surfaces of the body are for the most part harmless ; while cer- 
tain intestinal forms may even be useful in promoting digestion. 

Certain bacteria which do not often and some which never induce 
disease, find in or upon the human body such favorable conditions for 
their existence that they are commonly present there. 

The body is guarded in various ways from the incursions of patho- 
genic and other bacteria, which may be commonly present or only occa- 
sionally lodged upon its surfaces. Among the protective agencies of the 
body may be mentioned the firm, dense skin which while intact protects 
the interior from the entrance of almost all known micro-organisms ; the 
epithelial investment of the mucous membranes in several places swept 
by cilia ; the protected situation of most of the mucous surfaces, the anti- 
septic cpialities of some of the secretions, such as the gastric juice, etc. 

But notwithstanding the safeguards of the body against the access of 
micro-organisms, these do frequently enter ; this may occur in severe in- 

^ For a summary of facts concerning the bacterial flora of the body surfaces, con- 
sult M'elcJi, "Surgical Bacteriology," "System of Surgery by American Authors," Den- 
nis, p. 250 et seq. See also Ford, "The Bacteriology of Healthy Organs," Trans. Assoc. 
Amer. Phys., vol. xv., p. 389, 1900, Bibl. 

-For a resume of micro-organism in the air see Gottstein, Lubarsch and Ostertag's 
'•Ergebnisse," Jahrgang iv., pp. 87 et seq., 1897. 

■^ It should be remembered that the gastrointestinal canal, the lungs, and other vis- 
cera which are in communication with the exterior, although within the limits of the 
body, form still, strictly speaking, its outside, in distinction from the intimate recesses 
of the tissues in which the life processes go on. 



160 THE RELATIONS OF MICRO -ORGANISMS TO DISEASE. 

juries to the skin or mucous membranes or through very slight and un- 
noticed abrasions or other solutions of continuity. Entrance may be 
gained to the tissues through the minute ducts of the sebaceous or sweat 
glands; from the gastro- intestinal canal' and the respiratory passages 
and surfaces, either with or without obvious injuries to the investing 
epithelia. The role of insects in the conveyance of infectious agents is 
of great importance. ' Micro-organisms mary enter the body during intra- 
uterine life, also. 

When in one way or another bacteria or other germs have entered the 
tissues, they may encounter a series of obstacles to their spread or con- 
tinuance as well as to their proliferation there, even should the general 
nutritive conditions be favorable. In the first place the lymph- nodes 
frequently filter out of the tissue fluids micro-organisms which have 
entered them, holding them back from the general circulation or destroy- 
ing them.^ The power of certain of the body fluids and of living cells 
under favorable conditions to kill and dispose of germs, should these gain 
entrance through injuries or other structural lesions or functional dis- 
turbance in the barriers, is of great importance and will be referred to 
again. The elimination of micro-organisms from the body through its 
secretions,' such as urine, bile, milk, sweat, saliva, etc., is a matter of 
great significance, but one upon which the scope of this book does not 
permit us to enter. ^ 

The view has been recently advanced that with no apparent lesion 
or with but very slight lesions of the intestinal mucosa, bacteria in 
lai^ge numbers may gain access through this to the liver, where they may 
be destroyed or under certain conditions eliminated, either through the 
bile or into the body at large. ' 

Action of Bacteria and their Products in the Body. 

When bacteria do enter and grow in the body, the cells and tissues 
near them may show very^ marked alterations, due to their influence. 

^For bibliography concerning the permeability of the gastro-intestinal canal for 
bacteria refer to p. 523. 

^ Niittall, Johns Hopkins' Hospital Reports, vol. viii., p. 1, 1900. 

^ManfrecU, Virch. Arch., Bd. civ., p. 335, 1899, for a study of the germicidal and 
other action of lymph-nodes ; also Bezancon and Labbe, Arch, de Med. experimentale et 
d'Anat. path., t. x., p. 389, 1898. 

4 Consult Sherrington, "Experiments on the Escape of Bacteria with Secretions," 
Journal of Pathology and Bacteriology, vol. i., p. 258, 1893; Biedl and Kraus, Arch. f. 
exp. Path., Bd. xxxvii., p. 1, 1895, Bi'bl. ; Hintze and Luharsch, "Ergebnisse der allg. 
Aetiologie der Menschen- und Thierkrankheiten," 1896, p. 287. 

5 For a suggestive summary of the various factors which are or may be concerned 
in the protection of the body against the invasion and action of micro-organisms, see 
Meltzer, "Physiological Methods of Protection of the Body against BacteriaV' Trans, of 
the Congress of American Physicians and Surgeons, vol. v., p. 12, 1900, 

See also for the importance of a lesion in animal tissues for the lodgment and mul- 
tiplication of bacteria within it, Gheesman and Meltzer, Jour. Exp. Med., vol. iii., p. 
533; also on the significance of granulation tissue in wound infection, Afanassieff, Zieg 
ler's Beitrage, Bd. xxii., p. 11, 1897; also Cohbett and Melsome, Centralbl. f. Path., Bd. 
ix., p. 827, 1898, Bibl. ; also Jurgelicnas, Ziegler's Beitrage, Bd. xxix., p. 92, 1901, Bibl. 

^Adami, on "Latent Infection and Subinfection," etc., Journ. of the Amer. Med. 
Association, December 16 and 23, 1899. 



THE RELATIONS OF MICRO -OEGrANISMS TO DISEASE. 161 

The cells may be swollen, or their nuclei may disappear, and the proto- 
plasm may be converted into a mass of shining or coarsely granular 
particles, or may completely disintegrate. The intercellular substance 
near the bacteria may also soften and distintegrate. In a word, the 
tissue in their immediate vicinity is often found in a condition of necro- 
sis of one kind or another. The walls of blood-vessels near which they 
lie may be damaged and the blood which these carry may form thrombi. 
The bacteria may themselves enter the vessels and proliferate in the 
blood ; they may be swept away as emboli to remote parts of the body 
(Fig. 40, page 113), and establish new foci of bacterial proliferation and 
tissue necrosis — septiccemia. 

Some bacteria, instead of inducing a sim^Dle necrosis, incite at the 
same time, as we have already seen, a more or less intense inflammation 
(Fig. 11, page 111). This inflammation may be of a simple productive 
form, similar in its effects to that incited by the presence of any irri- 
tating foreign body ; or it may be active, progressive, and exudative in 
character ; or the bacteria may determine, in some way as yet unknown 
to us, very peculiar and characteristic inflammatory changes, which re- 
sult in the formation of new tissues of various kinds (see Tuberculosis). 
Some forms of bacteria find in the blood, others in the tissue spaces and 
lymph-vessels, the conditions most favorable for their proliferation. 

But the presence of micro-organisms themselves is not indispen- 
sable for the incitement of either local or general pathological processes. 
These may be induced by various chemical products eliminated or stored 
up in their protoplasm by the metabolism of the germs. These delete- 
rious bacterial products may, as we have already seen, be those alkaloidal 
substances called poisonous iDtomains or toxins, or they may be albumi- 
noid substances — toxatbumins or toxalhumoses.' Stored up in the proto- 
plasm of the germs themselves, this i3oisonous material has been called 
bacterio-protein. 

Some of the poisons act locally at or near the seat of their manufac- 
ture by the growing germs. Others gain access to the body at large and 
are widely distributed, inducing what may be called the i^henomena of 
septic intoxication — toxcemia. 

The phenomena of septic intcxication may be induced by the prod- 
ucts of bacterial growth outside of the body when these in considerable 
quantity are in any way taken into it. This is true not only of poisons 
elaborated outside the body by pathogenic bacteria, but also of many 
forms of bacteria usually harmless. Thus are caused many forms of 
food poisoning which simulate but are not actually infectious diseases, 
because there is no development within the body of the disease-inciting 
germs. 

Similar local and general effects may be induced in the body by other 
poisons than those of bacterial origin. Eicin and abrin, for example, 

' Much of the literature on this subject has been brought together by Vaaghan and 
Kovy, " Ptomaines and Leucomai'nes. " The general chemical relationship of bacterial 
products to other organic compounds is set forth mHallihurtorts "Text-Book of Chem- 
ical Physiology and Pathology." 
11 



162 THE KELATIONS OF MICKOOEGAXISMS TO DISEASE, 

well-kuowii vegetable poisons, aiul the venom of scorpions and of certain 
snakes are closely similar in their action to the toxins which the bacteria 
form either within or withont the body. 

It shonld be remembered in this connection that effects closely resem- 
bling those dne to bacterial or allied poison may be induced by toxic 
agents developed within the body as a result of defective elimination or 
faulty cell metabolism — auto- Intoxication (see p. 329). 

Thus the deleterious effects of i^athogenic bacteria upon the body are 
but in small measure simply mechanical. Local necrosis' and inflamma- 
tion, albuminous degeneration of cells, leucocytosis and other alterations 
of the blood, fever, structural lesions and functional disturbances in the 
nervous system, irregularities in the circulatory and respiratory mechan- 
isms, may follow the distribution in the body of bacterial toxins. 

Proofs of Infective Nature of Bacteria Found in the Body. 

It will be seen, from what has now been said of the bactci^'ia, that in 
different parts of the system in health, and in a large number of abnor- 
mal conditions, various forms of bacteria occur ; but it is quite e\ ident 
that the significance which we must attach to their mere j)resence varies 
greatly. In a large nund^er of cases, especially when on parts exposed 
to the air or in the gastro-intestinal canal, they are evidently of no more 
importance than so much inorganic dust. Vf hen, however, special forms 
of bacteria are uniformly present in connection with well-defined dis- 
eases, or in their lesions, the conjecture is certainly justified that the 
micro-organisms may have something to do with their incitement. Yet 
in all such cases we have to consider the possibility that it is the abnor- 
mal state of the bodj^ or the character of a lesion, brought about perhaps 
in other ways, which affords conditions suitable for the growth of bac- 
teria, and that these may consequently be iDresent in considerable num- 
bers, w^hile in the absence of such conditions they would be unable to 
develop. Even the constant occurrence in the body, in certain diseases, 
of bacteria which evidently jDroduce well-marked local effects, either 
inflammatory or degenerative, does not absolutely prove their etiological 
relationship) to the disease, although it renders it in a high degree prob- 
able. 

It is desirable in every case in which the evidence of the etiological 
relationshij) of a specific micro-organism to a disease is to be set forth, 
that we should be able to demonstrate the constant presence in the body 
of the special form of micro-organism ; obtain this by culture in a pure 
condition unmixed with any other living thing or with any chemical 
substance not belonging to it, and finally, by the introduction of the 
puiified organisms into a healthy animal, be able to produce the disease 
in some definite form. When all this is done, and not before, can we 
assert that the evidence establishing the causative relationship between 'a 

^ See Flexner, "The Pathology of Toxalbumin Intoxication," Johns Hopkins' Hos- 
pital Reports, vol. vi., p. 259, 1897. 



THE EELATIOXS OF MICEO-ORGAXISMS TO DISEASE. 163 

given form of bacteria and any special infections disease, is entirely at 
our command. 

But the fulfilment of these strict logical requirements is very difficult 
in many cases, and in some, api)arently, almost if not quite imj)ossible ; 
for we must remember, in the first place, that the lower animals, upon 
which alone, for the most part, inoculation exi)eriments are practicable, 
are apparently not subject to certain important diseases of man ; and, 
second, that they i^resent among themselves the most marked differences 
in the degree and manner in which they are affected by inoculation with 
pathogenic bacteria. Desirable as is the comj)lete fulfilment of the above 
requirements in e^ ery case, it must be admitted that a reasonable cer- 
tainty regarding the bacterial origin of a given disease may sometimes 
be arrived at without positive results from the inoculation of the bac- 
teria associated with its lesions. 

The complete demonstration which is desirable has as yet been fur- 
nished in but a moderate number of cases. In many others, however, 
enough has been done in the way of study and experimentation to render 
it altogether certain that the diseases are infectious and to establish 
beyond reasonable doubt the identity of the micro-organism or micro- 
organisms involved. 

Conditions Influencing the Occurrence of Infectious 

Diseases. 

It has beeji learned, as the result of a great deal of observation and 
experiment, that although certain diseases are always associated with the 
presence and growth in the body of particular species of micro-organ- 
isms, there are still various other accessory factors which have an im- 
portant bearing npon the inception and course of the diseases. Thus, 
while the x)resence in the body of a particular species of micro-organism 
is the most significant and fundamental of the determining agencies in 
the infectious diseases, the numbers in which they are present — i. e. , the 
size of the dose — and the varying virulence which the same species under 
different conditions possesses, as well as the varying capacity of resist- 
ance to the incursions of the germs which the body cells at different times 
and under differing conditions exhibit, are all factors of the greatest 
moment. 

Malnutrition, mental or physical overwork, injuries, bad hygienic sur- 
roundings, and intemperance, as well as many other conditions which favor 
deterioration in the general health, are often decisive factors in determin- 
ing the intensity or even the occurrence of the diseases due to bacterial 
incitement. It is thus clear that the action of a given germ in the liv- 
ing body depends only in part upon its intrinsic capacities — which in 
themselves are very variable — but also and in marked degree ui^on the 
capacities, also variable, which exist at the moment in the body cells 
among which the lot of the germs is cast. 

It should be always borne in mind that the human body is a great 



164: INFECTION AND IMMUNITY. 

aggregate of groups of co-ordinated cells which, under normal conditions, 
all act in harmony for the maintenance of the life and functions of the 
individual. The cells and cell communities in health not only do this, 
but they have the power of resisting and to a certain extent overcoming 
various deleterious agencies to which the body is more or less constantly 
liable. 

What we call hereditary or acquired predisposition to an infectious 
disease, such as tuberculosis for example, is simply a lack of the usual 
capacity of the cells of the body — whether through a structural or physi- 
ological fault we do not yet know — to cope with the destructive tenden- 
cies of the living micro-organisms when once these gain a foothold in the 
body. 

We thus see that, in studying the conditions under which infectious 
diseases occur, the work is by no means complete when the bacterial 
species which incites the disease has been discovered, but that then the 
more obscure determining and influencing agencies must be worked out 
in each case. 

Infection and Immunity. 

INFECTIOUS DISEASE AND THE NATURE OF INFECTION. 

Infectious diseases are those which are incited by the entrance into the 
body and proliferation there of pathogenic micro-organisms. Infection is 
the act or process by which such diseases are incited. 

In the more exact usage of the words infectious and infection which 
our new knowledge demands, it is customary and convenient to limit the 
term micro-organism to the fungi — bacteria, yeasts, and moulds — and to 
the i^rotozoa representing the animal kingdom, excluding altogether the 
entozoa and other animal parasites. ' 

The modern conception of infection implies the presence in the body 
of the living micro-organisms themselves, that is, of something capable of 
multiplication, or at least of reproduction and development, and not alone 
of the poisons which they may and usually do produce. It is customary 
to look upon the effects of the absorbed poison which micro-organisms 
furnish as intoxications, whether these poisons be formed inside the body 
in infectious diseases and in other conditions, or outside of it and subse- 
quently introduced. That condition in which there is evidence of wide 
distribution of pathogenic micro-organisms and their products in the 
blood is called septiccemia (see p. 179). 

It is evident from what has been said that infectious disease cannot 
exist without the presence in the body of micro-organisms. But, on the 
other hand, micro-organisms can and do frequently exist in the body 
without the incitement of infectious disease. Whether a micro-organ- 
ism be pathogenic or not depends upon the variable susceptibilities of 

- With this somewhat arbitrar}^ limitation, neither trichinosis nor scabies, for exam- 
ple, would be considered an infectious disease, althougli they are often for the lack of 
a distinctive word thus designated. 



INFECTION AXD IMMUNITY. 165 

the host as well as upon its own — also variable — nature and qualities. 
;No micro-organism is intrinsically pathogenic ; the very conception im- 
plies a relationshij). This obvious fact is overlooked by those who see in 
the micro-organisms alone the essential specific features of infectious 
diseases ; who would classify these diseases exclusively by the nature of 
their excitants, and who look upon the latter as the true '^causes'' of the 
phenomena through which disease is manifested (see p. 67). 

FORMS OF INFECTION. 

Mixed or Concurrent Infection, — It should be borne in mind that the 
body which is already the seat of an infectious disease is usually espe- 
cially susceptible to the action of other pathogenic germs, should these 
once gain entrance ; and also that the lesions which are associated with 
many of the infectious maladies afford portals of entry through the skin 
or mucous membranes to other micro-organisms, against the entrance of 
which the healthy body opposes most efficient barriers. In fact, we now 
know that the action of two or more i^athogenic micro-organisms in the 
body at the same time is of very frequent occurrence, many of the so- 
called complications of the infectious diseases being due to secondary 
infection with a new germ species. Numerous examples of this ''mixed '' 
or, better, "concurrent,^' infection are noticed in other parts of this 
book. ' 

. Many important facts have been revealed by the study of bacterial 
association in cultures as well as in infectious diseases of men and ani- 
mals which cannot here be considered.^ It may be said in general that 
in animals as in man concurrent infection with a second micro-organism 
increases the gravity of the original situation. On the other hand, cer- 
tain exi^eriments seem to indicate that sometimes the concurrent action 
of a second germ — strej)tococcus, for example, with the anthrax bacillus 
— may render a virulent organism comparatively innocuous. But the con- 
ditions of the experiments are in either case so complex that the full sig- 
nificance of many curious phenomena is not yet aiDparent. 

Congenital Infection. — Infection of the foetus through such lesions of 
the placenta as permit of the passage of pathogenic micro-organisms from 
the blood of the mother to that of the child is of occasional, but not fre- 
quent, occurrence. While the barriers against such transmissions are, 
under normal conditions, effective, disturbance in the placental circula- 
tion, lesions of the vessel walls or of the tissues and covering of the 
chorionic villi favor it. But infection may occur without demonstrable 
evidence of such lesions. Thus foetal infection is known to have occurred 
in various phases of suppurative inflammation, in tuberculosis, typhoid 
fever, anthrax, syphilis, the exanthematous fevers, etc. There is con- 
siderable evidence that rarely the tubercle bacillus may be transmitted 

^ For bibliograpliv of mixed infection see Bernlieim and Griiher, Lubarsch and 
Ostertag's "Ergebnisse," Jahrg. 2, for 1895. p. 1. 

^Consult Th. Smitli, Trans. Association American Physicians, vol. ix., p. 85, 1894. 



166 IXFECTION AND IMMUNITY. 

from mother to offspring, and remaining for a time inactive may later 
indnce the characteristic lesions.' 

Terminal Infection. — The victims of chronic disease of the heart, blood- 
vessels, kidneys, liver, etc., are particularly snsceptible to the incursions 
of pathogenic micro-organisms and to infectious diseases of one kind or 
another. Such persons, with or without definite lesions, are in fact liable 
finally to succumb to the comxDlicating disease. The phrase ^Henninal 
infection " has been ai)plied by Osier and others to this concurrence of 
diseases of such different nature, in which the chance infection of a \\\l- 
nerable organism is so apt to prove fatal. ^ 

Great care is, however, necessary in determining the significance of 
the various forms of bacteria which may be present in the body after 
death. Not only may bacteria develop to a considerable extent in the 
body during the hours which x)recede death when the natural protective 
agencies are halting or abeyant, but this may occur without such a re- 
action on the part of the body cells as is necessary to constitute an actual 
infection. Furthermore, multiplication and distribution of bacteria in 
the body after death is of frequent occurrence and must in every case be 
taken account of in weighing the evidence for terminal infection. ^ 

COM MUNIC ABILITY OF INFECTIOUS DISEASES. 

It is imi)ortant in j^ractical dealings with the infectious diseases to 
consider them in the light of the relative liability of transmission of the 
actually known or assumed micro-organisms from diseased to healthy 
individuals. 

In the finst place, it should be borne in mind that the lower animals 
are insusceptible to the ravages of some of the micro-organisms which 
readily incite infectious disease in man. Thus the lower animals are, 
so far as we know, naturally immune to syphilis. To certain diseases of 
the lower animals, on the other hand, man is not subject. But to certain 
other infectious diseases, tuberculosis for example, both men and lower 
animals are susceptible, and both are, in fact, under the prevailing con- 
ditions of modern life, frequent victims. 

So far as the liability to the transmission of the infectious agents from 
man to man is concerned, there is a very marked and significant differ- 
ence between the infectious diseases. It is common usage to speak of the 
transmission or communication of disease, as if disease were a self -exist- 
ent thing. This usage fosters much loose thinking. What we call dis- 
ease is a process involving a departure from, failure in, or perversion 
of normal physiological action, either in the material constitution or in 
the functional integrity of the living organism. When, therefore, we 

^ For bibliography and summar}^ of foetal infection see Lubarsch, "Ergebnisse der 
allg. Aetiologie der Menschen- und"^ Thierkrankheiten," Jahrg. i., p. 427, 1895; also 
Fischl, Grandier, Comby, and Marfan' s "Traite des Maladies de I'Enfance," t. i., p. 
454, bibliograplij^ 

^ For a study of this class of cases see Flexner, Transactions Association American 
Physicians, vol. xi., p. 229, 1896. 

^Consult Acharcl and Phulpin, Arch, de Med. experimentale, vol. vii., p. 25, 1895. 



INFECTION AND IMMUNITY. 167 

speak of the ti^ansmission or communication of disease, what we really 
mean is not that the disease, but the agent capable under suitable condi- 
tions of inciting the disease is transmitted or communicated. If we hold 
this obvious implication in mind, it is useful to group the infectious dis- 
eases of man into two great primary classes: 1st, Those which under the 
usual conditions of life are not readily communicable. 2d, Those which 
under the usual conditions of life ai^e readily communicable. 

But while, for convenience, we may speak of non-commiuucable and 
commiuucabJe diseases, we should remember that these two classes merge 
into one another, and that in fact the agents of infection may at least 
artificially in all cases be conveyed from one individual to another. It 
is only Avhen the conveyance under natural conditions occurs in a round- 
about way, or through intermediary agencies as in the case of malaria oi- 
yellow fever, that one may advisedly si)eak of non-communicable infec- 
tious diseases. 

Among the communicable infectious disease there exists the widest 
difference in the liabilitj^ to transmission under ordinary circumstances. 
Thus the infectious agents in smallpox and scarlatina are given off from 
the body under such conditions as render possible and frequent their 
direct transmission through the air to another individual. In syphilis, 
tetanus, and rabies, on the other hand, transmission of the infectious 
material is rare or impossible without a direct inoculation. 

Between these extremes the widest diversity exists in the liability to 
transmission of the infectious agents of the diseases of this class. In 
fact the liability to infection on the part of a healthy individual in the 
presence of a Adctim of infectious disease is largely dependent upon the 
intelligent care which is exercised in the disposition of the material con- 
taining the j)athogenic micro-organism which in one way or another the 
infected body sets free. 

So that while it may be useful to arrange the communicable infectious 
diseases in groui)s, or in such serial order as may indicate the degree of 
communicability of each under the ordinary conditions of life, it should 
always be borne in mind that this classification is not fundamental as is 
that by which the infectious diseases as a whole are set apart from other 
diseases, but is closely dependent w^on the sanitary conditions under 
which each case may be placed. Thus tuberculosis, or diphtheria, or 
pneumonia may be high on the list as readily communicable, if the pa- 
tient be housed in a crowded tenement with ignorant or careless attend- 
ance, while if subjected to the intelligent ministry of sanitary science 
these diseases may be accounted as relatively slightlj^ communicable. ' 

^ Before the knowledge of pathogenic micro-organisms had become precise, readily 
communicable diseases were called contagious in a rather loose and ill-defined way, and 
the unknown excitant was called the contagium. The word contagious is still vised, in 
various senses, to the detriment of science. We can get along well enough without it 
by the use of the word communicable as above indicated. But if it must still be cher- 
ished it might be wisely limited to the exanthemata, whose inciting agents are more 
readilj' and commonly transmitted through the air from the body of the patient than 
are those of any of the other infectious maladies. 



^^^^f^fms^ 



168 INFECTION AND IMMUNITY. 

IIVCMEUNITY. 

Mature and Forms of Immunity. 

We have seen that an infectious disease is one incited by the entrance into 
the hody and proliferation there of imthogenic micro-organisms, and that in- 
fection is the act or process by which such a disease is incited. 

The fact that all animals are not equally susceptible to the ravages of 
pathogenic micro -ox'ganisms, and that in man an individual and often a 
changing predisposition or invulnerability to the incursions of these or- 
ganisms exists ; the further observation that one attack of an infectious 
disease often x)rotects the victim for a longer or shorter time against a 
recurrence ; finally, the fact that recovery is ever possible when once 
self -multiplying disease -producing germs have obtained a foothold in the 
body^all these facts and observations are of such singular import and 
interest that, especially of late years, much study has been ex]3ended on 
the nature of the agencies which the body brings into play in establish- 
ing immunity in the face of microbic invasion, and in coping with the 
various deleterious factors at work when once a foothold is obtained. 
The scope of this book does not permit us to enter in detail into this most 
fascinating and important field. We can give only a brief summary of 
some of the more important features. 

Immunity is insusceptibility, or capacity for resistance on the part of the 
body, to infection or its effects. 

If we recall the ways in which bacteria damage the organism, it will 
be evident that immunity may be due to the fact that the micro-organ- 
isms in question simply do not proliferate in the body, failing, even 
should they gain entrance, to find the necessary conditions. On the 
other hand, though the conditions be in general favorable, substances 
may exist or be formed in the body which destroy the invading germs. 
In other words these may at once or soon be disposed of by germicidal 
substances, either in cells or in solution in the body fluids. 

Or, the toxic substances which micro-organisms set free, as in the proc- 
ess of their nutrition they decompose organic ingredients of the tissues 
or body fluids, may be rendered inert by further decomposition or com- 
bination with substances present or formed in the tissue fluids. Or, the 
cells which are susceptible to the presence of the toxins may become 
less vulnerable by adaptation to the deleterious effects of the latter. 
Thus by a total unsuitability of the tissues or of the general conditions 
to bacterial growth ; by destruction of the invading germs ; by neutrali- 
zation or destruction of toxins ; or, finally, by a capacity of resistance 
or tolerance won through adaptation to a new and intrinsically harmful 
environment, we may in a somewhat vague but still instructive way con- 
ceive of conditions which in a measure account for the known phenom- 
ena of immunity. 

Immunity from an infectious disease may be hereditary. Thus our 



INFECTIOX AND IMMUNITY. 169 

domestic animals enjoy a natnral or hereditary immunity from many of 
the infectious diseases of man.' On the other hand, immunity may be 
acquired. Acquired immunity may be secured by an attack of the disease 
from which the individual has recovered — natural immunization — or by 
the introduction into the body of some material which gradually dimin- 
ishes susceptibility without inducing distinct disease — artificial immuniza- 
tion. Acquired immunity may be transmitted from parent to offspring. 

Most of the infectious diseases appear to confer a certain degree of 
insusceptibility to subsequent attacks of the same disease, though this 
may be partial and temporary. But the exanthemata afford the most 
striking examples of acquired immunity after an attack of infectious 
disease. 

Let us now look more closely at some of the agencies through which 
the body may thus protect itself from the consequences of infection. 

It is well known that bacteria artificially introduced into the blood of 
animals may, after a short time, wholly disappear from the circulating 
fluid, and be found in large numbers in leucocytes and other cells. AVe 
have already seen in the study of inflammation (see p. 116) that certain 
cells of the body are capable not only of taking up micro-organisms 
which enter the tissues, into their protoplasm, but may there kill and 
perhaiDS digest them, and that thus the destruction of germs in the body 
may be brought about. This mode of destruction of micro-organisms, 
largely by leucocytes but also by other mesodermal cells, which when 
thus engaged are called phagocytes, plays a most im]3ortant part in the 
establishment of immunity. 

On the other hand, certain albuminous ingredients of the body fluids, 
'^a/^xi/is^' or "defensive proteids," have been shown to possess marked 
germicidal powers. 

While thus two fairly distinct influences are evidently of importance 
in enabling the body to resist the incursions of pathogenic germs — cellu- 
lar or "phagocytic" and what maybe called the "humoral'^ or chemical 
— it is obvious that ultimately whatever destructive power the body pos- 
sesses toward micro-organisms must be due, indirectly or directly, to cell 
activities. This phase of immunity has been characterized as anti-micro- 
bic or anti -bacterial immunity. 

Furthermore, the microbic toxins which are set free by the micro- 
organisms may, like other poisons, be eliminated together with the waste 
products of body metabolism through the kidneys, skin, etc. 

Artificial Immunization. 

General Methods and Principles of Artificial Immunization. — If we turn 
from the germicidal and eliminative phases of immunity just considered 
to the agencies through which either with or without the destruction or 

^ For a most suggestive and vahiable paper on the adaptation of patliogenic bac- 
teria to different species of animals see Tlieobald Smith, Pliiladelpliia Medical Journal, 
May 5tli, 1900. 



170 INFECTION AND IMMUNITY. 

inhibition of growth of the micro-organisms, artificial immunization may 
be secured, especially through the neutralization of the action of toxins, 
we encounter the results of a great amount of the most painstaking ex- 
perimental research. Briefly to summarize these, we find that artificial 
immunization can be accomi^lished by gradually rendering the body 
tolerant in one way or another to the presence of. the infective agencies 
without actually inciting the characteristic specific disease. 

I. In one class of procedures artificial immunity is secured directly or 
indirectly through the action in the body of bacteria or other microbes or mi- 
crobic poisons whose virulence has been in one way or another reduced but not 
rendered altogether inert ; or by the action on relatively insusceptible animals 
of microbes or microbic poisons of unimpaired virulence. 

1. Insusceptibility to particular forms of infectious disease may be 
conferred by inoculation with cultures of the germ inciting the infection 
whose virulence has been artificially reduced. This reduction of virulence 
of the micro-organisms may be accomplished in various ways — by culti- 
vation at temperatures above their optimum ; by successive inoculations 
into insusceptible animals; by prolonged artificial cultivation in the 
presence of oxygen; by exposure to certain inorganic chemical sub- 
stances, as the diphtheria bacillus to trichlorid of iodin, anthrax to bi- 
chromate of potash, etc. ; by exposure of cultures to organic extracts or 
products of animal or vegetable cell metabolism ; by drying (hydropho- 
bia), or by exposure to sunlight; and in other Avays. 

With the virulence of the micro-organisms reduced in varying degrees 
in one or other of the ways just mentioned, the gradual habituation of 
the bodies of animals to the presence of pathogenic germs may be pur- 
sued until cultures of full virulence are tolerated. 

2. Immunity may be conferred by the injection, in gradually increas- 
ing doses, of the metabolic products of bacterial growth, either with or with- 
out the dead bodies of the germs themselves — the bacilli of typhoid fever 
for example. The primary virulence of these usually toxic products of 
microbic growth may be in various ways diminished, by heating, by mix- 
ing with organic extracts such as that of the thymus gland, or with an 
inorganic chemical substance such as trichlorid of iodin, or by small 
doses of the already prepared antitoxin — see below. 

3. Immunity may be secured in some cases by the inoculation of ani- 
mals which are but moderately susceptible to the species employed, with 
small but increasing quantities of germs having unimpaired virulence. 
Under these conditions the animal becomes more and more unresponsive 
to the germ, until finally it may display no reaction after a quantity of 
the virulent culture which at first would have been inevitably fatal. 

Immunization in man by the direct use of microbes or microbic poisons 
or virus of diminished virulence has been largely practised in typhoid 
fever, cholera, and hydrophobia. 

II. In a second class of procedures artificial immunity is secured by the 
direct mingling of the body fluids from an already immune individual with 
those of the individual to be protected. 



INFECTION AND IMMUNITY. 171 

1. Extracts of various organs and tissues of animals suffering from 
infectious disease, rendered germ-free and injected into healthy animals, 
have been found in some cases to confer a certain degree of immunity. 

2. The blood serum of animals naturally immune to a particular in- 
fectious disease has been found on injection into those which are suscep- 
tible to the same disease to impart in some cases a certain degree of 
insusceptibility. 

3. The blood serum finally of animals which have been rendered in 
one way or another artificially immune to certain diseases, if introduced 
under proper conditions into another susceptible animal, has been found 
not only to confer a temporary immunity, but if administered to an 
already stricken individual to aid him in the most marked and efficient 
way to overcome the deleterious agencies at work. 

Antitoxic Substances : Practical Serum-Therapy and Preventive Inocu- 
lation. — The knowledge of this immunizing and curative action of spe- 
cially endowed blood serum has been most fully developed in diphtheria 
and tetanus. The application of a wide range of facts experimentally 
revealed in the lower animals^ has led to the opening of a new method 
for the prevention and control of infectious disease in man, which under 
the name of serum-therapy is not only full of promise but has already 
proved to be of inestimable practical value. 

The fact that many of the pathogenic micro-organisms act harmfully 
upon the body largely through their self -engendered toxins, and that the 
effect of the introduction of the blood serum of artificially immunized 
animals appears to be to counteract this deleterious effect, has led to the 
use of the word ayititoxin for the substance or substances, still but little 
understood, which the serum of the immunized animal has been found 
under these circumstances to contain. This phase of immunity in which 
the effect is reached through a counteraction of the effects of the toxic 
substances is called antitoxic immu7iity. 

These antitoxic substances appear to be most closely related to the 
globulins. They may exist in healthy individuals or animals, and their 
formation in immunization appears, therefore, to be due to an exalta- 
tion of normal cell functions about which we are at present almost 
wholly ignorant. ' 

The facts which have just been set forth indicate that in the artificial 
immunization we are bringing into play and reinforcing physiological 
capacities in cells which under natural conditions the body commands 
for ends which may not be identical, but are doubtless of similar purport 
to those which are accomplished in immunization. 

In the direct immunization of animals by the toxic products of germ 
metabolism, considerable time is consumed in rendering available the 
protective agencies which the body finally secures. On the other hand, 
in the employment of the blood serum of artificially immunized animals 
for i^rotective and curative purposes in man we make use of the accom- 
plished results of the protective mechanism of one animal for the more 

^ See Hiss and Atkinson, Journal of Experimental Medicine, vol. v., p. 47, 1900. 



172 INFECTIOIS^ AND IMMUNITY. 

direct, speedy, and certain protection of another, and this effect is se- 
cured without those evidences of profou^nd disturbance which the use of 
toxic agents frequently discloses. Moreover, the efficiency of the im- 
munizing or curative blood serum is directly proportionate, as a rule, to 
the degree of immunity which the animal from which it is derived enjoys, 
and upon the amount of serum, or, which is the same thing, the amount 
of antitoxin introduced. This substance, antitoxin, does not act appar- 
ently by directly neutralizing, in a chemical sense, the poison which is 
determining the manifestations of the infectious disease, but it appears 
to stimulate the body cells which constitute the natural protective 
mechanism of the stricken individual to greater activity or to more pur- 
poseful accomplishment. While some of the antitoxic substances at the 
same time inhibit the growth or kill micro-organisms, this is by no means 
always, or usually, the case. 

In diphtheria the perfection of the process of artificial immunization 
and the establishment of a precise and successful curative method ^ are 
the direct results of a long, patient, logical series of animal experiments 
with a definite end in view, and by the use of the absolutely identified 
and well-known germ which induces the disease. On the other hand, it 
is not a little curious that in smallpox and in hydrophobia effective methods 
of immunization should have been perfected without precise knowledge 
of the ndcro- organisms which incite the diseases, and yet by procedures 
which though somewhat empirically hit upon, are nevertheless in close 
accord with those which the most recent studies on immunity in general 
have shown to be effective. Thus in both smallpox and hydrojDhobia the 
material used for protective inoculation is that which has been artificially 
reduced in virulence ; in the one case — smallpox — by it passage through 
the body of a relatively insusceptible animal ; in the other — hydrophobia 
— by drying in the air: but in neither case do we yet know the excitant 
of the disease. 

The Specific Character of Artificial Immunization. — It is not yet possible 
to say in many cases to what extent the immunization effected in any of 
these various ways is specific. In some cases it appears to be so. That 
is to say, the protection which is afforded, for example, by an attack of 
diphtheria or by the gradually increased administration of the diphtheria 
toxin, or by the use of the immunizing serum, is limited to this particu- 
lar disease and is not to be secured, at least in such marked degree, by 
the use of other bacteria or bacterial products. In some instances, on 
the other hand, immunization against one micro-organism or its toxins, 
or against special toxic substances, affords protection against infection 
or intoxication by entirely different agents. Thus animals may be im- 
munized against anthrax by inoculation with bacillus pyocyaneus. 

It should be borne in mind, however much importance we may attach 
to the formation and action of the antitoxic substances, that these are not 
necessarily always present either in natural or acquired immunity to bac- 
teria or their toxins. Tolerance to bacterial toxins may be established, 
* See section on Diphtheria, p. 235. 



INFECTION AND IMMUNITY. 173 

as may toleranoe to other kinds of poisons, without the intervention of 
antitoxic or other chemical agents. 

The Complexity of the Processes Involved in Immunization. — It thus 
appears that Avhile we know a great deal about the ability of the living 
body to protect itself against the incursions of micro-organisms and the 
ravages of their poisons ; while a field is opened for the study of artificial 
immunization which is of the highest promise, both for the advancement 
of science and for iDractical benefit to the victims of infectious disease, 
we are yet very far from comprehending in their finer details the i^roc- 
esses by which immunization is secured. 

We do not know why the cells of certain animals or why different 
kinds of cells in the same animal are more susceptible than others to the 
presence of particular poisons ; why, for example, the rabbit is less sus- 
ceptible than man to morphiu, or why strychnin should affect the 
nerves while curare acts upon the muscles. We are even ignorant as 
yet in most cases of either the chemical or structural changes in cells by 
which the deleterious action of poisons is effected. This is indeed not 
surprising when we reflect that the processes which are involved are of 
the most subtle and complex nature, and that our knowledge of cell 
metabolism even under normal conditions is most crude and fragmentary, 
consisting largely in rather gross determinations of end products and leav- 
ing out of the account the numberless molecular transformations and 
combinations through which the life processes of the cell are carried on. 

The living body cell is very nicely adapted to its normal environment ; 
the living bacterium is almost equally sensitive to the conditions under 
which its metabolism takes place. Thus it is that when these subtle 
organisms react upon each other, we are wholly unable with our j^resent 
knowledge to follow the steps by which the more gross manifestations of 
disturbance which we call disease are reached. 

The scope of this work does not permit us even to review the various 
hypotheses by which one or another investigator has endeavored to ac- 
count for the evident phenomena of natural or artificial immunization. 
Some of the more obvious considerations have been here briefly set forth. 
It is certain, however, that in all its intricate details immunization is but 
the result of an adaptation of normal cell capacities to the special emer- 
gency which the introduction of a new environment involves. 



CHAPTER VIII. 

THE INFECTIOUS DISEASES. 

General Considerations. 

In the study of the infectious diseases it is especially important to 
bear in mind that the abnormal processes through which the disturbances 
incited by micro-organisms are manifested are processes of the body cells 
and not processes of the micro-organisms. The micro-organisms do 
indeed incite the train of phenomena by which the disease is mani- 
fested and the nature or ^^ species^' of the micro-organism may largely 
influence the character of the phenomena, but the stored-up energy 
which is released in this manifestation is body-cell energy and not 
that of microbic metabolism. The microbes are excitants of disease, 
but the disease is a performance of the body cells. If these obvious 
considerations be held in view, it will be convenient in considering 
certain of the infectious diseases to use the familiar and much abused 
term ^^ specific'' as indicative of those phases of abnormal body-cell 
performance which are apt to occur in characteristic ways in response 
to special forms of microbic stimulus. Thus the poisonous subtances 
which the tubercle bacillus builds up out of the organic material 
upon which it feeds are in part such as exert a peculiar influence upon 
connective-tissue cells, leading to their proliferation and the temporary 
formation of new tissue — the tubercle. This, together with associated 
action of the same or other metabolic products of the living bacillus, 
forms a group of lesions and disturbances which is characteristic of the 
action of the tubercle bacillus in the body. In this sense tuberculosis 
is a ^^ specific" disease. On the other hand, the poisons eliminated by 
the tubercle bacillus may incite responses on the part of the body cells 
which are practically identical with those which many other toxic sub- 
stances, both of bacterial and of other origin induce, fever, degeneration, 
etc. These manifestations of the action of the tubercle bacillus upon the 
living body cells are not '^ specific." 

In our study of the individual infectious diseases we shall encounter 
many examples of this variety in the effects which pathogenic bacteria 
induce — the more characteristic on the one hand, and on the other the 
more general responses which the body cells make to deleterious agents. 

Classification of the Infectious Diseases. — It is common to group dis- 
eases either from the clinical or the morphological or the etiological 
standpoint. But a complete rational classification of disease is not at 
present possible, because in very few diseases have we even an approxi- 



THE ITs^FECTIOUS DISEASES. 175 

mately complete knowledge of either the sjmi)toms, the excitants, or 
the morphology of the lesions. 

In the infections diseases as we now define them, the excitant is 
definite and in many cases known, bnt a classification based upon the 
character of the excitants alone wonld be, as Martins has nrged, a classi- 
fication of the micro-organisms and not a classification of the diseases. 
If every micro-organism capable of exciting disease always met in the 
body a similar response, the matter wonld be comparatively simple. 
Bnt the fact that the responses of the body cells to bacterial invasion are 
exceedingly varied, and that dissimilar organisms may evoke similar 
responses renders a simple etiological classification even of the infectious 
diseases unsatisfactory if not impracticable. Thus it is that it is con- 
venient to consider the infectious diseases in part together, in part in 
connection with the sx)ecial organs in which their more common and 
characteristic lesions are manifested. Such a classification of the in- 
fectious diseases as is here made is based in part upon similarity of 
lesions, in part upon the relationshii^s of the micro-organisms concerned, 
and may wisely be regarded only as a convenient form of catalogue. 

Groups of Bacterial Disease-Excitants. — One of the interesting results 
of the later studies of bacteria and their associations with the infectious 
diseases is the discovery that many micro-organisms which have been 
proved to be excitants of disease in men or in lower animals are closely 
related to forms which are not i^athogenic. So that we now recog- 
nize many bacterial groujDS which we are wont to characterize by the 
name of the pathogenic representative. Thus there are stai^hylococ- 
cus and streptococcus groups of closely similar organisms, most of them 
harmless to man. There is the colon bacillus grouj), embracing many 
closely related forms difficult to identify. The tubercle bacillus grouj), 
the dij)htheria bacillus group, the actinomyces or streptothrix group, are 
other examples of this relationship. ' The more these related forms are 
studied, the more evident it becomes that in very slight physiological 
variations may lie the difference between pathogenic and non-pathogenic 
forms, and that equallj" slight variations in the susceptibility of the host 
may be of corresponding significance. 

In the arrangement and associations of the infectious diseases consid- 
ered in this section, the existence of these bacterial groups will be fre- 
quently recognized. 

SUPPURATIVE AND ALLIED FORMS OF INFLAMMATION. 

We have seen in an earlier part of this book that in various kinds of 
injury to the living tissues there may be a series of responses on the part 
of the body cells which constitute or give rise to the phenomena and 
lesions of inflammation. One of these forms of tissue resi:)onse to injury 
is called supjmmtion or suppurative inflammation. 

^ This grouping- of related forms, frequently with special reference to the qualities 
of particular species as excitants of disease, has been especially worked out by Kruse. 
See Fliigge's "Mikroorganismen," Bd. ii 



176 THE INFECTIOUS DISEASES. 

We have seen that the characteristic feature of suppurative iuflam- 
mation is the collection at or near the seat of injury of leucocytes, mostly 
of the polymorphonuclear type. These leucocytes, attracted through 
chemotaxis, emigrate from the smaller vessels and gather in the tissues. 
Here they may proliferate ; through their phagocytic powers they may 
directly or indirectly destroy living micro-organisms ; by means of fer- 
ments which they elaborate, they may soften and remove dead tissues ; 
or they may themselves succumb to the action of j)oisons or other local 
conditions inimical to their life. While, to a limited extent, a suppura- 
tive inflammation can be incited by chemical agents, such as ammonia, 
turpentine, etc., in most cases it is incited and sustained by micro-organ- 
isms or by poisons which these micro-organisms set free as the result of 
their own metabolism or by the decomposition of substances in the tis- 
sues or the tissue fluids. 

Before considering in detail the characteristics of the various forms 
of micro-organisms which may act as excitants of suppurative inflam- 
mation, it is necessary for us to survey the various phases which this 
process presents under different conditions. 

In the first place while the emigration, proliferation, and gathering 
of leucocytes is the most characteristic feature in this form of inflam- 
mation, these are always associated with the accumulation of more 
or less fluid transudate from the blood-vessels and often with the for- 
mation of fibrin. These, the leucocytes, the serum, and the fibrin, 
constitute the exudate. Furthermore, associated with the accumulation 
of the exudate there may be albuminous degeneration and necrosis of 
cells and tissue of the affected part or of the formed elements of the 
exudate itself. Finally, a proliferation of the fixed cells of the 
affected region frequently accompanies the exudative phases of inflam- 
mation and may dominate the processes when regeneration and repair 
are under way. 

Although the processes involved are esentially the same, it has been 
found convenient to attach special names to various topographic forms 
of suppurative inflammation, the differences depending largely upon the 
origin, situation, extent, and complications of the primary lesion, some- 
what, however, upon the qualities fixed or variable of the infecting mi- 
cro-organism. Thus a suppurative inflammation involving the serous 
surfaces and resulting in the accumulation of a purulent exudate in the 
serous cavities, such as the pleural and the pericardial, is called empyema. 
An exudative inflammation of the mucous membranes with a marked 
emigration of leucocytes from the vessels of the submucosa is called a 
purulent catarrh or blennorrhoea. 

Pustules are superficial collections of purulent exudate in the skin. 
The result of a localized suppurative and necrotic inflammation starting 
usually in the hair follicles of the skin is called ^furuncle or cay%uncle, 
dei^ending upon the extent of the lesion. Ulcers — in whatever way 
originating — (see p. 90) may be the seat of suppuration, the exudate 
passing off upon the free surfaces. 



THE INFECTIOUS DISEASES. 



177 




Fig. 86.— Pus Cells in Suppurative Ix- 

FLAMMATION. 

Some of the cells show the marks of ne- 
crosis and disintegration with fragmenta- 
tion of the nuclei, etc. 



A diffuse infiltration of the subcutaneous or deep fibrous tissue or of 
the interstitial tissue of the viscera with exudate is colled 2)hIe(/mon. If 
in this phlegmonous inflammation there be much serous fluid associated 
with the cell accumulation, as is commonly the case in the earlier stages 
of the process, the condition is often 
named purulent cedenia. When, on the 
other hand, there is a more or less 
circumscribed collection of purulent 
exudate in the depth of the tissues or 
organs, associated with necrosis and flu- 
idification of the tissues involved, it is 
customary to call the result of the proc- 
ess an abscess. 

In some phases of exudative inflam- 
mation, particularly those involving the 
serous surfaces, the exudates often occur 
together in the most variable propor- 
tions; they are formed under the in- 
fluence of the same agents and frequently an exudate at first simply serous 
in character becomes fibrinous or purulent or both together. 

It will thus be seen that the exudate which is formed in suppurative 
inflammation varies considerably in its composition and structure. 
Primarily, pus consists of an albuminous fluid containing leucocytes, 

some mononuclears, most of them 
,-" V , polymorphonuclears (Fig. 86). 

^^^ ^ AVhile the exudate is in the tissue 

and the conditions are favorable, these 
cells may be alive and without struc- 
tural abnormalities. But often, and 
esi)ecially in accumulations, they pre- 
sent various phases of degeneration — 
albuminous or fatty — or of necrosis 
and disintegration. It is on account 
of their relative frequency and abun- 
dance in purulent exudates that the 
leucocytes are regarded 2)ar excellence 
as pus cells. But other cells may be 
1) resent in pus, thus in inflammation 
of the serous membranes, such as the 
j)eritoneum, pleura, etc., the exfoli- 
ated and proliferated mesothelial cells 
may furnish no small part of the cel- 
' ' hilar content of the exudate. In in- 

flammation of the mucous membranes also, the epithelial cells, either 
new-formed or simply exfoliated, may be abundant. Furthermore, pus 
may contain a variety of chemical substances and formed elements de- 
pending upon the place of its formation or accumulation. Thus mucus, 
12 









•*v. 




^rw 



Fig. 87.— Staphylococcus Pyogenes Au- 
reus, IX and Amoxg the Pus Cells, from 
AX Abscess of the Kidney. 



178 THE INFECTIOUS DISEASES. 

fibrin, cell and tissue detritus, fat, and micro-organisms may be inter- 
mingled with the pus cells. 

The bacteria which are found in the various phases of suppurative 
inflammation may lie free in the interstices of the tissue with the exu- 
date, or they may be in part within the cells which have gathered 
about them (Fig. 87). Both within and without the cells the bacteria 
may present those structural alterations which denote their death and 
degeneration in the struggle for existence to which the two forms of liv- 
ing beings, the microbes and the body cells, are subjected under the 
conditions which mark infection. The local and systemic reaction, on 
the other hand, and the cell necrosis which so frequently follows the 
growth of microbes in the body are expressions of an unfavorable envi- 
ronment to which the body cells as individuals and the body as a com- 
posite organism are subjected, and to which they may successfully react 
or under unfavorable conditions may succumb. ^ 



TOXiEMIA. 

While the various forms of exudative inflammation just described are 
more or less circumscribed, the soluble toxins which are formed at the 
seat of local bacterial growth may, without the dispersion of the germs 
themselves, be diffused through the blood and the other fluids of the 
body, giving rise to the symptoms and lesions of toxcemia — fever and vari- 
ous other forms of functional disturbance, albuminous degeneration of 
the viscera, focal necroses, petechial haemorrhages, thrombosis, leuco- 
cytosis, chromatolysis of the ganglion cells, etc. 

Of these alterations in the body which are of frequent occurrence in 
many forms of toxaemia, whether induced by bacterial or other kinds of 
poisons,^ the only one which demands special notice here are the focal 
necroses. These usually small, often sharply circumscribed areas of 
dead tissue may be present in any of the viscera, but are often most 
abundant and conspicuous in the liver. ^ They vary considerably in ap- 
pearance, depending upon the stage of the tissue involvement. The cells 
in the affected area may be swollen, the cytoplasm more transparent than 
normal, while the nuclei may remain unstained with the usual dyes or 
show various phases of fragmentation or disintegration; or they may 
disappear altogether. Again, the cells in the involved areas may become 
more coarsely granular than is normal, may undergo a change similar to 
that seen in coagulation necrosis and with destruction of the nucleus may 
form deeply staining, irregular clumps or masses, or may disintegrate 
(Fig. 88). 

^ For an exhaustive review of suppurative inflammation from the modern stand- 
point with bibliography consult Janowski, Ziegler's "Beitrage zur path. Anatomie," 
etc., Bd. XV., p. 128, 1894. 

^See for effects of abrin and ricin intoxication Flexner, Journal of Exp. Med., vol. 
ii., p. 197, 1897; also Midler, Ziegler's "Beitrage," Bd. xxvii., p. 331, 1900, Bibl. 

2 It seems probable that this marked localization of the action of a soluble poison in 
the tissue fluids may be due to some local vulnerability or susceptibility induced per- 
haps by limited vascular disturbance or by nutritional defects otherwise induced. 



THE INFECTIOUS DISEASES. 179 

Associated with or following these changes there may be a gathering 
of leucocytes about and within these necrotic areas, so that the foci may 
present the appearance of little abscesses or masses of lymphoid tissue. 
Finally, these necrotic areas may undergo repair and be replaced by 
small masses of cicatricial tissue. ' 

SEPTICiEMIA AND PYEMIA. 

Bacteria as well as their toxins may be distributed from a local portal 
of entry or an infected region throughout the body, not only inciting 
general functional and structural changes, but when the bacteria lodge 

- ■ -■" " " ■ '. ' ' >'-^ 



©' 



• • <3^^ • ■' 



» ,, 



VA ■■♦ V v: • : ^ ■ ^S •?'- :■ (i 

■ ' ® .' ^ '' ^ ^" 

FlG. 88.— FOCAL NECROSIS IN THE LlVEH INDUCED BY TOXIC MATERIAL OF BACTERIAL ORIGIN. 

in various situations giving rise by new local proliferation to fresh foci 
of inflammation. 

It is customary to designate the condition in which bacteria as well 
as their toxins are distributed through the body by the blood and lymph 
channels as septiccemia. When fresh suppurative foci develop as the re- 
sult of this distribution, the condition is called pywmia. 

The terms septicaemia and pyaemia are survivals of a nomenclature 
adapted to the period before the nature of the excitants of infectious 
disease was definitely known. The manifestations of septicaemia were 
then attributed to the presence of putrid material in the blood. Pyaemia 
expressed the belief that the lesions characterizing this condition were 
due to the presence of pus in the blood. The term hactericemia is some- 
times and more correctly used to indicate the presence of bacteria in the 
blood, but the old words with their new implications and limitations are 
still commonly employed.'^ 

^ For a comprehensive study of focal necrosis and other associated lesions in certain 
forms of toxaemia, consult the excellent study of Flexnei\ "The Pathology of Toxal- 
bumin Intoxication," Johns Hopkins' Hospital Reports, vol. vi., p. 259, 1897, Bibl. 

'-^ It has long been known that persons who have received injuries or wounds rriay 
suffer from constitutional symptoms, among the most marked of which may be fever, 
and develop local or disseminated lesions. To designate the condition of these patients 



180 



THE INFECTIOUS DISEASES. 



The term pyaemia, as will be seen, indicates a clinical and anatomical 
phase of septicfemia. 

The new foci of suppuration in pyaemia are called metastatic abscesses, 
and in distribution these may bear an obvious relationship to the seat of 
the primary lesion. Thus, in suppurative processes in the intestinal 
tract, metastatic abscesses are liable to occur in the liver. From sup- 
purations in the skin, bones, muscles, etc. , infectious emboli may be 
transmitted to the lungs and lead to infarctions and abscess ; or, passing 
these organs, the germs may induce multiple abscesses in the kidneys 
and in other viscera. 

It should be remembered that the point of introduction into the body 
of the offending germs may be wholly concealed and not associated with 







Fig. 



-Micrococci in Masses in the Fibrinous Exudation of pyemic Pleurisy. 



any form of demonstrable external lesion. This is often called crypto- 
genetic pyaemia or septico -pyaemia. 

After death from septicaemia and pyaemia there is a considerable 
variety in the post-mortem appearances. 

There are cases in which there are no recognizable gross lesions. 

There are cases characterized by early post-mortem decomposition ; 
post-mortem staining of the tissues ; congestion of the lungs, stomach, 
intestines, and kidneys; extravasations of blood in the serous mem- 
branes; swelling of the solitary and agminated lymph-nodules in the 
small intestine ; swelling of the spleen and albuminous degeneration of 
the liver and kidneys ; chromatolysis of the ganglion cells of the brain 
and cord. 

There may be localized inflammations. The joints, the connective 
fcissue around the joints, the pleura, the pericardium, the peritoneum, 

the terms pyaemia, septicaemia, septico-pyaemia, pyo-septicaemia, ichoraemia, inflamma- 
tory fever, surgical fever, traumatic fever, suppurative fever, puerperal fever, and 
purulent infection have been used. 



THE INFECTIOUS DISEASES. 181 

the pia mater, and the connective tissue in different parts of the body 
may be inflamed. These local inflammations are usually purulent, ex- 
cept in the serous membranes, where the j)rincipal inflammatory product 
may be fibrin (Fig. 89). The veins in the neighborhood of the wound 
may contain softened, purulent thrombi, without infarctions in the vis- 
cera while there may be inflammation of the joints and serous membranes. 
On- the other hand, with the venous thrombosis there may be infarctions 
and abscesses in the viscera; local inflammations of the joints and serous 
membranes may be present or absent. While thrombi are often formed 
in the veins near the wound, they may be situated in veins at a distance, 
and sometimes, although infarctions and abscesses be present, no thrombus 
can be discovered. The veins may be distended by the thrombi or contain 
only small coagula. The different kinds of thrombi, and the varieties 
of emboli and infarctions which they produce, are described in the section 
on Thrombosis, p. 72. Leucocytosis usually accompanies pyaemia and 
septicaemia as well as the suppurative process with which they are asso- 
ciated. Studies of the blood in various forms of septicaemia are numerous 
and instructive, but we cannot consider them here. ^ 

Various lines of research on minute changes in cells which bacterial 
and other poisons may induce justify the expectation that more and 
more we shall be able to associate characteristic groups of symptoms in 
toxaemia and septicaemia for which there is now no morphological basis, 
with well-defined cell alterations. Among the most striking of the toxic 
cell lesions thus far studied in septicaemia and bacterial toxaemia are those 
involving the cytoplasm of the ganglion cells (see Nervous System). 

THE PYOGENIC BACTERIA. 

^\Tiile many species of microbes are capable under favorable condi- 
tions of inciting supj)uration and other forms of exudative inflamma- 
tion and may when they or their toxins are disseminated in the body 
give rise to toxaemia, septicaemia, and pyaemia, there are two forms 
which, on account of their early discovery and their relative frequency, 
are commonly considered asj9«r excellence ^^ pyogenic^' bacteria. These, 
which are called Stapliylococcus and Streptococcus, we shall consider first. 

Chaeactees of Staphylococcus Pyogenes. 

The Staphylococcus pyogenes aureus (Micrococcus pyogenes aureus) (Fig. 90) is a 
relatively small coccus, the individuals varying, however, considerably in size (0.7 to 
1.2 11 in diameter). In its growth it does not show a characteristic grouping, but grows 
in irregular masses and heaps (the somewhat crude resemblance, when studied imder 
a cover glass, to a bunch of grapes gave rise to the generic name) ; sometimes, however, 
pairs and groups of four or short rows of the cocci are seen. The germ is readily stained 
by the anilin dyes, and does not lose its color in Gram's method of staining. It does 

^Consult WJiite, Journal of Experimental Medicine, vol. iv., p. 425, 1899; also: 
Adami, Journal of the xAmerican Medical Association, December 16th and 23d, 1899. 
Both have bibliography. 



182 



THE INFECTIOUS DISEASES. 



not show spontaneous movement, and, like other spheroidal forms, does not appear to 
develop spores. It is quite tenacious of vitality, surviving long drying and degrees of 
heat and cold and an exposure to chemical bactericides to which many pathogenic germs 
readily succumb. It grows well at ordinary room temperature in such artificial culture 
media as nutrient -gelatin, agar, beef tea, and milk, and on potatoes, forming somewhat 
voluminous masses of culture. It rapidly fluidifies gelatin, 
coagulates milk, and in the various media develops a yellow- 
ish-white or a deep golden-yellow color, whence its specific 
name, aureus, and its common name, "golden coccus." Its 
color-producing capacity is subject to wide variation. 



m 



Fig. 90.— Staphylococcus 
Pyogenes aureus. 



From a beef-tea culture. 



Effects of Staphylococcus Pyogenes in the Body. — 

The virulence of cultures of Staphylococcus pyo- 
genes obtained from different sources varies con- 
siderably, but in general, suppuration is not readily induced in the 
lower animals by its subcutaneous injection. Liability to suppuration 
is greatly increased by mechanical or chemical injury to the tissues with 
which the germ is brought in contact. Injection of a virulent culture 
into the ear vein of the rabbit is usually followed by multiple abscesses 
in the kidneys and muscles, by suppuration of joints, etc. 

In man this coccus grows readily and rapidly, and may induce necro- 
sis and exudative inflammation, especially the suppurative phases (Fig. 




Fig. 91.— Masses of Micrococci in a Blood-Vessel of the Kidney, Inducing a Small Abscess. 

From a case of pyaemia. 

Around the dilated and partially necrotic blood-vessel in which the bacteria lie is an area of necrotic 
tissue and a small-celled infiltration or zone of pus. The bacteria are not difEerentially stained. 

91). The lesions which it induces are apt to be circumscribed. It may 
induce pustules, boils, and abscesses, and various suppurative inflamma- 
tions of the viscera and serous membranes, joints, bones, endocardium, 



THE INFECTIOUS DISEASES. 183 

etc. These effects may be induced by the staphylococcus alone or by 
it in association with other species of germs. 

Staphylococcus pyogenes aureus incites these changes in the body in 
virtue of certain toxins or toxalbumins which are produced as the re- 
sult of its metabolism, and which are either at once set free or stored up 
in the body of the germs until their release by disintegration after the 
death of the germs. The special power of the staphylococcus to cause 
the gathering of leucocytes is apparently due to the marked chemotactic 
powers of some of the proteid substances in its protoplasm. 

It may enter the body through wounds, small or large, of the skin or 
mucous membranes. The possibility of its entrance through uninjured 
surfaces has been demonstrated. In many cases we are quite unable to 
trace it mode of access. ^ A\Tiile in the natural course of events this germ 
tends to die in the body, it may yet remain for a long time alive. 

It is widespread in inhabited regions, especially in towns, being fre- 
quently found on the surface of the body, and in the saliva, particularly 
of those with acute or chronic catarrh of the upper air passages. As the 
result of the filthy habit of indiscriminate public spitting, it is common 
in the dust of hospitals, houses, towns, public conveyances, and places 
of public assembly. "" 

Other Forms of Staphylococcus. 

Staphylococcus iryogenes albus. — This appears to be a variety of the Staphylococcus 
pyogenes which does not develop the yellow color in cultures. It is of frequent oc- 
currence both in connection with the aureus and alone. Its action on the body is similar, 
but it has seemed to many observers to be in general less virulent. 

StapJiylococcus epiclermidis albus. — This coccus has been described by Welch as of 
frequent occurrence in the epidermis, and although of rather feeble pyogenic power, 
yet seems frequently to cause small stitch-abscesses and moderate suppuration along 
drainage tubes. Welch regards it as possibly a variety of Staphylococcus pyogenes 
albus. 

Other forms of staphylococcus have been described — S. salivarius pyogenes, S. 
cereus albus and flavus — but they are apparently of little pathological significance. 



Chaeactees of the Steeptococcus Pyogenes. 

The Streptococcus pyogenes (Micrococcus pyogenes) is distinguished morphologically 
from the cocci just described by the marked tendency which the individuals exhibit, 
when growing, to hang together in longer or shorter chains (Fig. 92). It is like the 
Staphylococcus pyogenes, immobile, and stains easily in the same way. 

It grows readily, but more slowly than Staphylococcus pyogenes on the ordinary 
culture media. It does not fluidify gelatin, on which it grows as small, inconspicuous, 
grayish-white colonies. On the surface of agar plates kept in the thermostat at 37'' C. 
for twenty -four hours, the small grayish colonies usually show^, under the microscope, 
loops and fringes of the chain-like cocci extending off from the borders. The growth 

^ For a resume of the role of S. pyogenes aureus in the skin disease, with bibliog- 
raphy, see White, Boston Medical and Surgical Journal, vol. cxli., p. 235, 1899. 

- For bibliography of S. pyogenes aureus, consult monograph by i\ Lingelslieim, 
"Aetiologie u. Therapie der Staphylokokken Infectionen," in Beitr. zur Exp. Therapie, 
Heft i. a, 1900. 



184 THE INFECTIOUS DISEASES. 

on potatoes is inconspicuous. In nutrient broth it usually forms delicate; flocculent 
masses, which cling to the sides of the tubes, leaving the fluid clear. Occasionally the 
masses of streptococci are dense and compact. Not infrequently the growth is diffused 
through the nutrient broth, rendering it turbid. When in vigorous growth it coagu- 
lates milk. 

There is considerable difference in the tenacity with which, in broth cultures of 
streptococci from different sources, the individual cocci cling together, so that in one 
set of cultures the chains may be very long, in another short. It has been thought by 
some observers that this difference is so constant as to justify special names for these 
growth variants of the streptococcus, and they have been called respectively Strepto- 
coccus longus and Streptococcus brevis. The growth in small dense masses has given rise 
to the name Streptococcus conglomeratus. It is questionable, hoM^ever, whether these 
___ names should be regarded as implying more than 

j^ ^■ a a»J^*'Si^f % rather inconstant growth varieties. 




\^ • \ Effects of Streptococcus Pyogenes in the 

jNk t^ •'/ •'"'%,_, t^^ Body. — Streptococci which give evidence of 

- vNi'V *^«e^**% little virulence in animal inoculation are very 

? ^ • V»***«^*^ common in the mouths of healthy persons. 

y J^^ • ^ The significance of these germs in healthy 

^ „„ „ „ mouths is not yet clear. 

Fig. 93.— Stkeptococcus Pyogenes. •^ 

From a broth culture. The results of animal inoculation with the 

Streptococcus pyogenes are in general simi- 
lar to those with the Staphylococcus pyogenes aureus. The strepto- 
coccus is very frequently associated with the staphylococcus both in its 
distribution outside the body, in healthy persons, and in disease. In 
general it may be said that the streptococcus incites those forms of sup- 
puration and fibrino- purulent inflammation which tend to spread both 
locally and through metastasis. 

Streptococcus pyogenes has been found either alone or in association 
with staphylococcus in a large number of suppurative processes in vari- 
ous parts of the body, the condition in some cases receiving special names, 
in others not. Thus in boils and carbuncles, in abscesses and phlegmons, 
in herpes, impetigo and i)anaritium, in phlebitis and lymphangitis, in 
erysipelas, in suppurative inflammation of various mucous and serous 
membranes, and in some forms of pneumonia, one or other or both of 
these germs are frequently concerned. ^ 

One of the most important features of the relationship of Streptococ- 
cus pyogenes to man is the frequency with which it enters as a concur- 
rent pathogenic agent in already established infectious diseases due to 
other forms of micro-organisms. Thus some of the most serious com- 
plications to which the victims of scarlatina, diphtheria, typhoid fever, 
and pulmonary tuberculosis are liable are due to the action of the strep- 
tococcus in the body rendered unusually vulnerable by the existence of 
another form of infection. 

Streptococci which upon their isolation from the body in suppurative or other in- 
fectious processes are very virulent, usually, and sometimes very quickly, partially or 
wholly lose this virulence under artificial cultivation. On the other hand, cultures of 

1 Anaerobic streptococci have been found by various observers in abscesses and 
other forms of suppuration of which they are apparently the excitants. 



THE INFECTIOUS DISEASES. 



185 



streptococci which have largely lost virulence under artificial cultiA^ation or whose 
initial virulence was slight, may experience a great exaltation of virulence by a long 
succession of inoculations from animal to animal.^ 

The metabolic products formed by virulent streptococci growing in nutrient 
broth, when freed from the germs by filtration, have been found to induce in animals 
the symptoms of toxaemia. The results of preliminary experiments on immunization 
with these toxic products of S. pyogenes and the use of the blood serum of the immune 
animal for therapeutic purposes appear to be promising. But the practical value of 
the so-called streptococcus antitoxin is at this date not fully determined. 

ERYSIPELAS. 

Erysipelas is a diffuse inflammation of the skin and subcutaneous 
tissue which tends to spread, and is characterized locally by swelling of 
the tissue and a bright-red color of the integument. It is usually accom- 







.«»••* «♦ 

-t"-— 



"firoiier^""-— >--i ■ 



Fig. 93.— Erysipelas of the Skix. 
Showing streptococci in the lymph spaces. 



panied by constitutional disturbances, the most marked of which is fever. 
The morphological changes at the seat of lesion, as we see them after 
death, vary considerably in different cases and in different stages of the 
disease. The redness of the skin usually disappears after death. But 
the tissues may be swollen by the accumulation of serous fluid. This 
fluid may be nearly transparent, or turbid from admixture with pus cells 
(Fig. 93), Pus cells may infiltrate the tissues either sparsely or in dense 
masses. Fibrin may be present, abscesses may form. Sometimes vesi- 
cles or scabs are found on the surface, or the affected region may become 
gangrenous. Aside from the local lesions, there may be toxaemia marked 
by petechife in the serous membranes, swelling of the spleen, focal necro- 
ses, and albuminous degeneration in the kidneys and liver. 

The most common excitant of erysipelas is Streptococcus pyogenes. ^ 

^ For bibliography of streptococcus consult monograph by v. Lingelslieim, " Aetio- 
logie u. Therapie d. Streptococcus-Infection," Beitr. z. exp. Therapie, Heft 1, 1899; 
for a study of the action of streptococcus toxin on various parts of the body see Honien 
and others, Ziegler's "Beitrage," Bd. xxv., p. 159, 1899. 

2 In the early days of modern bacteriology the " chain " coccus which was discov- 
ered in the exudate of erysipelas was thought to bear a peculiar relationship to this 
clinical form of phlegmonous inflammation and was called by FeTdeisen Streptococcus 
erj^sipelatis, but it has now been definitely identified with the S. pyogenes. 



186 THE INFECTIOUS DISEASES. 

This organism may be present in large numbers in the lymph-vessels, 
especially in the borders of the inflamed region. The reasons for the 
clinical peculiarities of this phase of inflammation are not yet very clear. 

INFECTIOUS PSEUDO-MEMBRANOUS INFLAMMATION OF MUCOUS 
MEMBHANES. (Pseudo-Diphtheria ; Diphtheroid- Angina ; Membranous 
Angina.) 

Under a variety of conditions, as during scarlatina and measles, 
whooping-cough, typhoid fever, etc., or entirely apart from any compli- 
cating disorder, an acute exudative inflammation of the mucous mem- 
branes, especially of the upper air passages, occurs, which is associated 
with and is apparently induced by the growth of Streptococcus pyo- 
genes. There may be much or little fibrinous exudate ; there may in 





A ^ 







Fig. 94.— Pseudo-Membranous Inflammation of Trachea. 

In this case there is purulent infiltration of the mucosa and submucosa, and of portions of the mucous 
glands, a, False membrane ; b, portion of intact epithelium ; c, infiltration of the mucosa with Qbrin ; d, 
portion of mucous gland infiltrated with pus. 

early stages, or even throughout, be none at all. The pellicle when 
formed may be loose or adherent, sharply circumscribed or tending to 
spread. The submucous tissue may show little change, or may be con- 
gested and (Edematous, or may be the seat of suppurative inflammation 
(see Fig. 94), necrosis, or gangrene. The process may be confined to 
the tonsils. A\Tiile under these varying conditions the inflammatory 
process is usually a local one and runs its course with or without the 
symptoms of septicsemia, occasionally the streptococcus which enters 
the blood may induce the lesions of pyaemia. On the other hand, it 
may by aspiration gain access to the lungs and induce varying phases 
of complicating broncho -pneumonia. The Staphylococcus pyogenes is 
not infrequently associated with the streptococcus in these lesions, but is 
not apparently of primary significance. Simulating very closely, as it 



THE INFECTIOUS DISEASES. 187 

does in many cases, both the local and general phenomena of diphtheria, 
this disorder has formerly been confounded with it, and has been only 
recently recognized as a distinct phase of disease. It is now most fre- 
quently called pseudo-dii^htheria. It seems in part to cover the condi- 
tion formerly known as croup, in part those cases formerly thought to be 
mild diphtheria. In many phases of acute angina, and in many cases of 
follicular tonsillitis, streptococci have been found in large numbers. 
Other bacteria, either alone or in association with the pyogenic cocci, 
may be excitants of pseudo -membranous as well as simple angina. 



OTHER BACTERIA WHICH ARE FREaUENT EXCITANTS OF 

SUPPURATION. 

While the Staphylococcus pyogenes and Streptococcus pyogenes are 
the most common excitants of local suiDpuration with and without toxaemia 
and septicaemia, such conditions, as we have seen, are not infrequently due 
to other micro-organisms. Among these we may mention here as the 
more common and important : Micrococcus lanceolatus, the gonococcus, 
Micrococcus tetragenus, Bacillus pyocyaneus, the colon and the typhoid 
bacillus, the bacillus of glanders, the tubercle bacillus, the x>iieiiiiio- 
bacillus of Friedlander, the diplococcus of cerebro- spinal meningitis, 
Bacillus pyogenes foetidus, and Actinomyces with its related forms. 

In some of these organisms the pyogenic qualities in their relation- 
ships to human infections are most conspicuous ; in others, the reaction 
of the body to their presence is such as to justifj^ a special name. The 
latter is particularly noteworthy in the case of the pueumococcus, the 
gonococcus, glanders, typhoid, and tubercle bacilli, diplococcus menin- 
gitidis, and actinomyces. 

Many other micro-organisms niaj be excitants of suppurative inflam- 
mation in man as well as in the lower animals under experimental 
conditions, but this exceptional reaction of living tissues does not fall 
within the scope of this work, which deals j)rimarily with such tissue re- 
actions as may occur under the natural conditions of life. 

The Bacillus Coli Communis and the Colon Group. 

The baciUus coli communis is an organism so frequently present in the 
intestines under normal conditions as to be commonly called the '^ colon 
bacillus. ^^ It is a motile, aerobic, asporogenous bacillus considerably re- 
sembling in general form the typhoid bacillus (see p. 204). It has been 
repeatedly found under such conditions in connection with suppurative 
processes as to justify the belief that it is often their excitant. 

It has been found in various forms of peritoneal supi^uration, both 
with and without such lesions of the intestine as would obviously permit 
of its egress ; in appendicitis ; in suppuration about the gall ducts ; in hsem- 
orrhagic pancreatitis ; in inflammatory processes in the genito- urinary 
apparatus ; in the pericardium and pleura. Although a usual inhabitant 



188 THE INFECTIOUS DISEASES. 

of the intestinal canal, the Bacillus coli is often extremely virulent when 
once it gains access to the tissues of the body, especially if these be 
otherwise injured beforehand. Local infection with this organism is 
often associated with serious toxaemia and septicaemia. Intravascular 
injections of virulent cultures in rabbits are usually followed by symp- 
toms and lesions of septicaemia. Introduced subcutaneously and intra- 
peritoneally, it may excite local suppuration or sero -fibrinous inflamma- 
tion, often haemorrhagic in character, terminating fatally.' 

There are so many organisms so closely resembling the colon bacillus 
in their morphological and biological characters that it has been found 
convenient to consider them as possible variations of one form and to 
speak of them collectively as the ^^ colon group." The differentiation 
between the individual members of this group and between these and the 
typhoid bacillus has presented many difliculties to bacteriologists and 
given rise to much technical finesse. It is now possible to differentiate 
between the members of the colon group and the typhoid bacillus and 
to separate them in pure cultures. 

The Bacillus Pyocyaneus. 

This has been known for several years as an organism occasionally 
found in pus to which in its growth it imparted a greenish color. 
Charrin in 1889 established the significance of the organism as an exci- 
tant of suppurative inflammation and various manifestations of septi- 
caemia to which he gave the name '^ Maladie pyocyanique. " Since this time 
many cases have been reported in which the Bacillus pyocyaneus, either 
alone or in association with other organisms, has been found ; for ex- 
ample, in purulent otitis media, angina, endocarditis and pericarditis, 
suppurative inflammation of the urinary tract, meningitis, broncho-pneu- 
monia, gastro -intestinal disturbances in infants and adults, and in lesions 
of the skin as well as in systemic infections arising from primary local 
suppurative inflammation. The green color is not always present in the 
lesions, being first developed in the cultures or in experimental animals. 

The occurrence of the organism is on the whole infrequent. It was 
found by Jadowski twice in systematic cultures of the exudate from two 
hundred cases of suppurating wounds. Barker found it in eleven out of 
eight hundred cases in which systematic cultures from autopsies were 
made. It was found in three out of one hundred cases examined by 
Lartigau. Among the more marked lesions which may be present in 
cases of pyocyaneus infection, we may mention albuminous degeneration 
in the viscera, focal necroses, haemorrhages, local hyperplasiae (Oertel's 
lesion) in the lymph-nodes and nodules throughout the body, and espe- 
cially superficial, circumscribed or diffuse necrosis and ulceration in the 
intestinal mucous membrane.^ 

1 For details concerning B. coli, with bibliography, consult Mace, " Traite de Bac- 
teriologie," 1901. 

2 For a critical summary of the cases with original studies and bibliography consult 
Lartigau, Philadelphia Medical Journal, September 17tli, 1898; also Journal of Experi- 
mental Medicine, vol. iii., p. 595, 1898. 



THE INFECTIOUS DISEASES. 189 



Characters of the Organism. 

This organism is from 1.5 to 2 [x long, sometimes grows in short chains, is motile, 
and decolorizes bj' Gram's method. It grows readily on artificial media, usuall}^ devel- 
oping a greenish pigment. It liquefies gelatin. Subcutaneous injection of cultures in 
rabbits may be followed by local suppuration, by hgemorrhagic oedema, and by septi- 
caemia. 

Bacillus Pneumonia (Feiedlandee). 

In a small proportion of cases of lobar and lobular pneumonia, and 
in a few cases of exudative inflammation of the pleura, pericardium, 
meninges, and middle ear, this bacillus has been found. It is sometimes 
found alone, but in pneumonia is frequently associated either with the 
Micrococcus lanceolatus or with the pyogenic cocci. It has been found 
in the nasal secretion and mouths of healthy persons. While belonging 
definitely among the bacilli, it so frequently occurs in the form of very 
short rods or ovals or short chains that it was formerly thought to belong 
among the cocci. 

It seems highly probable rather than proven that it may be at least 
I)artially responsible for the lesions with which it is infrequently asso- 
ciated in man. This germ was formerly believed to be of great impor- 
tance in connection with acute lobar pneumonia, and for a time was 
generally spoken of as the pneumococcus of Friedlander. It is now 
known not to be a coccus, and is certainly of subordinate if at all of 
serious importance in the induction of inflammation of the lungs. ^ 

Micrococcus Tetragenus. 

This organism has been many times found about the mouth and re- 
spiratory tract, especially in connection with suppurative processes. It 
has been found also in metastatic abscesses. While not very virulent it 
is apparently an occasional excitant, either alone or with other organ- 
isms, of suppuration. ^ 

Characters of the Organism. 

It is a coccus about 1 // in diameter, usually occurring in groups of four. These 
tetrad groups may be encapsulated. It stains by Gram's method, and is readily culti- 
vated on artificial media. It forms a dense whitish growth on gelatin which it does 
not fluidify. Septicsemic lesions with local suppuration may be induced in guinea-pigs 
by subcutaneous injection with cultures. 

The Proteus Group of Bacilli. 

This is a large and in the economy of nature an important group of 
bacilli much concerned with the putrefactive processes. 

^Howard, Philadelphia Medical Journal, vol. i., p. 336, 1898; Leon, "Le bacille de 
Friedlander," These, Paris, 1897. 

For a study of this and related organisms, see Strong, Journal Boston Society, vol. 
iii., p. 185. 

-For resume of the significance of M. tetragenus and for bibliography, consult 
Lartigaii, Philadelphia Medical Journal, April 22d, 1899. 



190 THE INFECTIOUS DISEASES. 



Characters of the Group. 

Tlie bacilli of this group may be aerobes or facultative anaerobes. They are of 
medium size, asporogenous, and while staining readily with ordinary dyes are apt to be 
decolorized by the Gram method. While the organisms of this group are bacilli, they 
often present considerable variation in form as they grow, sometimes being very short 
so as to resemble cocci, sometimes forming threads which may be so bent as to suggest 
spirals. Their growth on solid media is especially characterized by the tendency to 
send runners from the central growth out into the surrounding media, thus establishing 
secondary growth centres. They are particularly sensitive to environment, so that 
physiological as well as morphological variations are frequent. It is for these reasons 
that the name Proteus has been given to the group and to various species. The limita- 
tions of the named species are, however, in many cases quite ill defined. 

One of the most common forms has been called Froteus vulgaris. 
While this bacillus is very widespread, it is only occasionally the exci- 
tant of pathological processes in man, and then almost always in concur- 
rence with other organisms, usually the pyogenic cocci. Under these 
conditions a suppurative inflammation with foul exudate is apt to de- 
velop. Thus it has been found in purulent peritonitis and endometritis, 
in pleurisy and in phlegmonous inflammation in various parts of the 
body. Although this bacillus is not apt to grow in the human body, 
except in association with other micro-organisms which may damage the 
tissues or in tissues already vulnerable from injury, it may in the blad- 
der independently incite an exudative inflammation. In animals, sub- 
cutaneous injection of the pure culture in considerable quantity may 
lead to abscess, while the soluble products of broth culture may induce 
toxaemia. 

Several other forms of Proteus, as well as closely related species, 
have been found in human lesions for the most j)art suppurative and 
necrotic in character and these, in some cases, have been conclusively 
shown to be the excitants of the pathological processes, but the scope of 
this work does not permit further details. ' 

Among the other bacteria which commonly induce local suppuration, 
with or without toxaemia and septicaemia, some are of frequent occur- 
rence as excitants of such well-marked and more or less characteristic 
forms of disease as have long been recognized clinically and have re- 
ceived special names, such as pneumonia, gonorrhoea, cerebrospinal men- 
ingitis, etc. These will be in part considered in the section dealing with 
the organs in which their more characteristic lesions are manifested. 



ACUTE LOBAR PNEUMONIA AND OTHER INFECTIOUS DISEASES 
INDUCED BY THE MICROCOCCUS LANCEOLATUS (Diplococcus 
Pneumoniae). 

Micrococcus lanceolatus is frequently spoken of as the ^'pneumococcus 
of Frankel, '^ because its significance and life history in connection with 

' These may be found in Kruse's article on "The Bacilli " in Flugge's " Mikroorga- 
nismen," last edition. 



THE INFECTIOUS DISEASES. 191 

acute lobar pueumonia were first demonstrated by him. ' It is commonly 
called simply the ^^pneumococcus.^^ 

Characters of the Micrococcus Lanceolatus. 

During their development these germs are distinctly spheroidal; but in their 
mature condition they are apt to become slightly elongated or oval and are often a little 
broader at one end than at the other, assuming a lanceolate form. They are vary apt 
to occur in pairs, and frequently are seen in short chains, rarely in long chains. Very 
frequently, when growing in the living animals, the pneumococcus is surrounded by a 
distinct, homogeneous capsule of varying thick- 
ness (see Fig. 95). This capsule does not, as a rule, ^ 
develop in artificial cultures. The coccus itself is jff ^ ^ 
readily stained by the anilin dyes and retains the ^ ^ 
stain by Gram's method; the capsule is not easily ma^ w 
demonstrated except by special staining methods. 

The pneumococcus has no spontaneous move- ^^ ^^ 0^ 

ment and grows but feebly at ordinary room tem- 
perature. It grows much better at blood heat, 

forming on the surface of blood serum or on very ^^f • 95.-Micrococcus Lanceolatus 
,. , ^, „ ,. , . 1 . ^ . ^ -1 (Pneumococcus) with Capsules. 

slightly alkalme glycerm-agar plates famt grayish, 

dewdrop-like, inconspicuous colonies, somewhat Stained by Welch's method, 

similar to those of Streptococcus pyogenes, but 

usually more delicate. In beef tea it forms at body temperature a faint whitish sedi- 
ment with slight turbidity of the fluid. As a rule, the cultures are prone to lose soon 
their virulence and to die ofC early, but the virulence may be maintained by successive 
inoculations in the rabbit. The organism may remain alive for a long time dried in 
the sputum, in one set of experiments for more than seventy days. 

The pneumococcus injected subcutaneously, while virulent, into mice and rabbits 
may induce a rapidly fatal septicaemia, often with little marked anatomical change, 
save enlargement of the spleen. Sometimes there are necrotic foci in the liver, fibrin 
in the glomeruli of the kidneys, fatty degeneration of the heart. Suppurative inflam- 
mation at the seat of inoculation and elsewhere may follow. The blood and viscera 
may show under these conditions numerous cocci, mostly with capsules, or they may 
be confined to the seat of inoculation. Cultures which have been reduced in virulence, 
so as not to cause early death by septicaemia, may, when introduced into the trachea of 
rabbits, induce a fairly typical lobar pneumonia ; especially if these animals are made 
vulnerable by cold or by other agencies which impair the integrity of the blood or other 
tissues.^ Different species of animals show marked differences in vulnerability to the 
effects of the pneumococcus. 

This germ is the exclnsive inciter of typical acnte lobar pneumonia in 
man. It appears to act, in part at least, by the development of an albu- 
minous poison which has been tentatively called pneumotoxin. ^ It would 
seem to be the pneumotoxin which induces the symptoms in acute lobar 
pneumonia indicative of systemic poisoning, since the bacteria them- 
selves are usually confined to the lungs. 

^ It was discovered by Sternberg in saliva, and its pathogenic power demonstrated 
some years before its full significance in connection with pneumonia was understood. 

■^ For reference to experimental pneumonia see p. 459. 

'^ The observations of the Klemperers and others suggest the possibility that at a 
certain period of the disease the blood or body juices are capable of developing a sub- 
stance antidotal to this pneumotoxin, the potency of the former beiiig signalized by the 
so-called "crisis." Satisfactoiy applications of this alleged " pneumonia antitoxin " in 
therapeutics have not yet been made. 



192 THE INFECTIOUS DISEASES. 

For a more detailed description of these lesions of pneumonia, and an 
account of other bacteria which may be present, see p. 450. 

In addition to its more common effect in inducing lobar pneumonia, 
the pneumococcus is frequently the excitant of exudative inflammationin 
other parts of the body, either in connection with or without a primary 
lobar pneumonia. Thus it has been repeatedly found in pleuritis, otitis, 
meningitis, empyema, pericarditis, endocarditis, and in peritonitis. It 
has also been found in abscesses of the viscera and in exudative inflam- 
mation of the joints. Leacocytosis usually accompanies infection with 
the x)neumococcus. 

It is a frequent inhabitant of the mouth, even in health. It has 
been found in the mouths of about twenty per cent of healthy persons 
examined. It is thrown off in the sputum in lobar pneumonia, and no 
doubt from these sources in the dried condition, as dust, furnishes the 
infectious agent which in favoring conditions of the body lights up the 
inflammatory process in the lungs. ^ 

For staining tlie pneumococcus with its capsule the method suggested by Welch ^ 
gives the most satisfactory result. 

The exudate containing the germ is dried and fixed upon the cover glass in the 
manner described on page 150. It is now treated with glacial acetic acid, which is at 
once drained off and replaced by anilin-gentian-violet solution (page 150), this being 
drained off and renewed several times until the acetic acid is displaced. The specimen 
is now washed with a two-per-cent solution of sodium chlorid, in wiiicli it may be cov- 
ered and studied. 

Such specimens are not usually suited for permanent preservation, although occa- 
sionally after drying and mounting in balsam the capsules retain their color. Annoying 
color precipitates frequently interfere with full success by this method. 

The pneumococcus maybe stained in sections by Weigert's modifications of Gram's 
method with preliminary contrast stain (see page 150). By this method the fibrin in 
the pneumonic exudate is also stained. 



GONORRHCEA AND OTHER INFLAMMATORY LESIONS INDUCED BY 
THE MICROCOCCUS GONORRHOSiE (GONOCOCCUS). 

The Micrococcus gonorrhoew (gonococcus) is most commonly found in 
the exudate of gonorrhoeal inflammation of the mucous membranes, es- 
pecially of the urethra. It may be free or enclosed in leucocytes or 
other cells (Fig. 96), within or between the epithelial cells. The organ- 
ism may be distributed from the seat of primary lesion, giving rise to 
gonorrhoeal arthritis, to malignant endocarditis, to exudative inflamma- 
tion of the pleura, and to inflammatory processes in other parts of the 
body. ' 

The gonococcus may in the primary as well as in the secondary lesions 
be associated with the '^pyogenic cocci, ^' the colon bacilli, or other micro- 
organisms. These associations have been observed in cases of pyaemia 

1 Ottolenghi, Centralbl. f. Bacteriologie, Abth. i., Bd. xxv., p. 120, 1899. 
- Welch, Johns Hopkins Hospital Bulletin, vol. iii., p. 128, 1892. 
^Consult, for cases and bibliography, Young, "Welch Anniversary Contributions 
to the Science of Medicine," p. 677, 1900; also: 

Elting, Albany Medical Annals, March, 1900, Bibl. 



THE INFECTIOUS DISEASES. 193 

following gonococcal infection. The gonococcus is usually most abun- 
dant in the urethra during the acute stage of the inflammation. But 

long after the organisms have disap- 

. , peared from the urethral discharge 

" * they may be present in small num- 

""; / ^^ .. ^, bers in the deeper portions of the ure- 

^"\,-\. " thra or in the prostatic secretions 

"''^/v ,-„-» .^ whence under favoring conditions a 

4 V, "" ' > "- I fresh infection may arise. In the 

^''•-*»" ' J*;^' ^ female the inflammation, through the 

': -* **"•.." transportation of the gonococci, may 

yy "",':•', ' %, extend to the vagina and uterus and 

\ ^ \> '' •* „*' into the Fallopian tubes. The germs 

"'» ' " may enter the peritoneum, inducing 

^ r^ ,, " , ^ exudative inflammation. Hvperplasia 

Fig. 96.— Micrococcus Gonorrhce^ in Cells. j i^ f 

— specimex from the Urethra. and Suppuration of lymph nodes near 

the inflammatory region may occur. 
Gonorrhceal conjunctivitis is similar in origin and character to the in- 
flammation of the urethra. 

Characters of the Gonococcus. 

Tlie gonococcus is apt to occur in pairs, the apposed sides being more or less dis- 
tinctly flattened (Fig. 97). It stains readily witli the anilin dj^es, and differs from most 
known cocci which might be mistaken for it in that it is decolorized by the iodin solu- 
tion in the Gram method of staining. It is well after the decolorization hy this 
method, and before mounting in balsam, to make a contrast stain with a dilute aqueous 
solution of Bismarck brown. Then the gonococci will be of light-brown color, while 
most other germs will retain the violet color. 

The gonococcus does not grow at ordinary room temperatures nor on the ordinary 
solid or fluid culture media. It ma}^ however, be cultivated at the temperature of the 
body on human blood serum or on a combination of this with agar. Heiman has found 
that it grows readily on the clear exudate or transudate 
from the pleural cavities in man when this is mixed 
with peptonized agar.' 

In this "chest-serum agar" the surface growth of • " - «§ c 

the gonococcus is in the form of small circular, sharp- 9 ^ %^*f # ^^ 

edged, slightly raised, nearly transparent colonies, •••<!► •^ 

coarsely mottled in the central portion, finely granular 

toward the borders. The life of the colonies under arti- Fig. 97.-Micrococcus Goxor- 
ficial culture is short, but by frequent transference to ^"^^ (Gonococcus). 

fresh media it may be maintained indefinitely and grad- ^^^ culture, 

ually adapts itself to the artificial environment. It is 

probable that the organism has no natural habitat outside the bodies of human beings. 
The lower animals are not, as a rule, susceptible to inoculations of the mucous mem- 
branes with the gonococcus, but suppurative inflammation has been induced in mice 
and guinea-pigs by intraperitoneal injections. 

Inoculations of pure cultures of the gonococcus upon the urethral 
mucous membranes of man have been repeatedly made and were fol- 
lowed by a characteristic catarrhal inflammation. Thus the evidence is 

1 Heiman, Medical Kecord, June 22d, 1895, Bibl. 
13 






194 THE INFECTIOUS DISEASES. 

complete that the gonococcus is an excitant of the inflammation with 
which it is so constantly associated. But in what measure this germ, in 
what measure others are responsible for the complicating inflammations 
when both germs occur together, is yet to be determined. 

Inasmuch as one or more forms of cocci and dii)lococci occurring in 
the normal and in the inflamed urethra are morx^hologically similar to 
the gonococcus, great caution should be exercised in doubtful cases in 
deciding upon the nature of suspicious micro-organisms in urethral dis- 
charges or other exudates. But the pronounced tendency of the gono- 
coccus to gather within cells ; the sometimes conspicuous but often ill- 
defined flattening of the apposed sides of the gonococci ; the decolorization 
by Gram's method, which leaves most other germs apt to be associated 
with the gonococcus still stained, and whenever practicable the artificial 
culture characters — these all should be considered in the summary of 
evidence. ' 

ACUTE CEREBRO-SPINAL MENINGITIS. 

This is an acute infectious disease of which the characteristic lesion 
is an exudative inflammation of the pia mater of the brain and cord. 

As a rule the inflammation of the pia mater results in a large pro- 
duction of serum, fibrin, and pus, which infiltrate the pia mater and ac- 
cumulate in the ventricles, so that the gross appearance of the brain is 
characteristic. The exudation is especially abundant at the base of the 
brain and over the x>osterior surfaces of the cord. In children the dis- 
tention of the lateral ventricles with purulent serum may be a marked 
feature, while in adults the quantity of serum is apt to be small. ^ 

While the above are the characteristic lesions of this disease, there 
are a number of secondary or associated septicsemic or toxsemic lesions 
in different parts of the body. There may be subserous punctate haem- 
orrhages in the endocardium ; petechige in the skin ; hyalin and granular 
degeneration in the voluntary striated muscle ; occasional multii^le ab- 
scesses in various parts of the body ; suppurative inflammation of the 
joints; albuminous degeneration of the heart, liver, and kidneys; and 
hyperplasia of the gastro -intestinal lymphatic apparatus and of the 
spleen. 

Cerebro- spinal meningitis may occur by itself or in connection with 
some other acute infectious disease, such as acute lobar pneumonia, 
mycotic ulcerative endocarditis, pyaemia, multiple suppurative arthritis, 
otitis media, puerperal fever, typhoid fever, etc. 

It may be epidemic, the lesions, however, being essentially similar to 
those in the sporadic form. 

1 Von Eibler, Centralbl. f. Bakteriologie, etc., Bd. xix., p. 120, 1896. For sum- 
mary of current work on the gonococcus with bibliograJDhy consult Neisser and ScMffer, 
" Ergebnisse der allg. Aetiologie der Menschen- u. Thierkrankheiten, " Jahrg. I. , Abth. 
1, p. 477, 1896. 

A comprehensive bibliography may be found in an article by Elting, Albany 
Medical Annals, March, 1900. 

2 For further details of the lesions in exudative meningitis, see Nervous System. 



THE INFECTIOUS DISEASES. 195 

Bacterial Excitants. — In sporadic cerebrospinal meningitis the strepto- 
coccus and staphylococcus pyogenes, micrococcus lanceolatus, ' the in- 
fluenza bacillus, the typhoid bacillus, and the gonococcus have been 
repeatedly found in the exudate. Other bacteria have been described. 

In epidemic cerebrospinal meningitis, a micro-organism has been re- 
peatedly found, called by Weichselbaum the Biplococcus intracellularis 
meningitidis, which is clearly one of the chief if not the sole inciting factor 
in the disease. It is found in the purulent exudate of the meninges in 
large numbers, and is usually within the leucocytes or pus cells. 

Characters of Diplococcus Intracellularis Meningitidis. 

It is an oval diplococcus not staining by Gram's method. Its growth on artificial 
media is meagre. It forms small transparent colonies on glycerin-agar at 37^ C. which 
soon die out without frequent transplanting to fresh media. It does not grow at room 
temperature. Animal experiments are on the whole confirmatory of the belief in its 
pathogenic activity. 

This organism closely resembles the gonococcus in morphology and 
considerably so in culture, and they are evidently closely related.^ 



GLANDERS. 

Glanders is an infectious disease incited by the presence and growth 
in the body of the Bacillus mallei. 

It is most common in the horse, affecting the mucous membrane of 
the nose (when involving the skin the disease has been called /«?'<??/), and 
can be communicated to man and to certain other of the domestic ani- 
mals by direct or accidental inoculations. 

The disease in man is most frequent in those who come much into 
direct contact with horses. The seat of primary local infection is most 
often the skin, more rarely the mucous membranes about the nose and 
mouth. 

The local lesions are similar in man and the lower animals. In the 
presence of the Bacillus mallei there is usually a circumscribed or more 
rarely a diffuse infiltration of the tissue with leucocytes and young con- 
nective-tissue cells. These whitish foci of cell accumulation may be 
small and to the naked eye resemble miliary tubercles ; or, . they may be 
larger and nodular. The tissues about them may be infiltrated with 
blood. But the accumulated cells are apt in the presence of the bacilli 
to become necrotic and disintegrate and thus lead to smaller and larger 
abscesses, or, if near the surfaces, to ulcers. If they occur on mucous 
membranes these lesions are often accompanied by intense diffuse catar- 
rhal inflammation. 

As the glanders nodules soften, the bacilli are apt to diminish in 

^ For bibliography of pneumococcus meningitis see Levi, Arch, de Med. Exp., t. ix., 
p. 49, 1897. 

^ For a study of cases with bibliograph}^ consult Flexner and Barker, American 
Journal of the Medical Sciences, vol. cvii., pp. 155 and 259, 1894; also Councilman, Mal- 
lory, and Wright, " Special Report of the State Board of Health of Massachusetts," 1898. 



196 THE INFECTIOUS DISEASES. 

number or in the capacity to stain, so that it may be possible to detect 
their presence only by inoculation or culture methods. 

The disease may begin at a single point, so that it may be mistaken 
for a carbuncle or gangrenous erysipelas. But the infection is apt not 
to remain local; the bacilli, finding their way along the lymph channels 
into various parts of the body, set up fresh foci of inflammation and 
necrosis. Then the skin may be covered with a pustular eruption; 
furuncles, carbuncles, and abscesses may form beneath the skin and in 
the muscles. ^N^odules are found in the nasal mucous membrane, the 
lungs, kidneys, testes, spleen, and liver. The joints may be inflamed, 
and there may be osteomyelitis. Leucocytosis may accompany infection 
with the B. mallei. 

The glanders infection may, however, pursue a more chronic course, 
with hard, persistent nodules and sluggish ulcers. Under these condi- 
tions the detection of the bacillus in the tissue by a simple morphologi- 
cal examination may be difficult. 

While some forms of glanders nodules somewhat resemble in gross 
and microscopic appearance certain forms of miliary tubercles, the ab- 
sence in the former of coagulation necrosis and of giant cells, and the 
tendency to rapid disintegration and softening in the latter will usually 
suffice for the distinction between the two sets of lesions. But the 
demonstration of the bacilli characteristic of each is in all cases decisive. 

Characters of the Bacillus Mallei. 

The Bacilhis mallei is a slender bacillus proportionately thicker than the tubercle 
bacillus, with rounded ends, occurring singly or in pairs (Fig. 98). It stains easily 
with the anilin dyes, but readily gives up the color in presence of even feeble decoloriz- 
ing agents such as dilute alcohol or acids. It is left decolorized by 
^^\A ^^ Gram's method. When stained, uncolored areas are apt to remain 
jf Sflk^if'^ in the body of the germ. Whether these are spores or not is not 
V^* fO ^1 yet definitel}^ determined. 
f^tW^^ III the tissues the bacilli may be stained with Loffler's alkaline 

methylene blue. 
Fig. 98.— Bacillus The glanders bacillus grows readily on almost all of the ordi- 

Mallei. nary artificial culture media, and best at blood heat. The growths 

on solid media are apt to be viscid. On potatoes it forms in two 
or three days an abundant j^ellowish pellicle which in a few days darkens and finally 
becomes brown in color. It gradually loses its virulence in successive generations of 
artificial cultures. The germ is easily killed by moist heat, but may remain alive in 
a dried state for months. Field mice and guinea-pigs are very susceptible to infection 
with the Bacillus mallei, and after inoculation develop highly characteristic local and 
general lesions. 

In cases in which an early diagnosis is imperative it is well, in addition to the mor- 
phological examination and cultures of the suspected exudate, to inject a small amount 
into the peritoneal cavity of a male guinea-pig. If the virulent glanders bacilli be 
present, within two or three days the testicles will swell and develop an intense sup- 
purative inflammation. 

As the glanders bacillus grows in nutrient broth a proteid substance — or substances 
— develops, which when concentrated by evaporation of the broth is called mallein. 
This substance prepared and administered to horses suffering from glanders, as tuber- 
culin is prepared and administered to tuberculous cattle (see page 225), gives a similar 
temperature reaction, and is thus an important diagnostic agent. 



THE INFECTIOUS DISEASES. 197 



Other Bacilli Related to Bacillus Mallei. 

Several bacilli, apparently related to the B. mallei, have been found in various 
lesions in men and lower animals. Thus an organism called Bacillus 2)seudotiibercidosis 
has been found in certain nodular lesions somewhat resembling tubercles which are 
especially frequent in rodents. B. pseudotuherculosis liquefaciens has been described in 
a series of cheesy nodules of the peritoneum, pancreas, and liver in man. In this group 
also belong organisms which have been found in noma. 

Chancroid. 

In the lesion of '"''soft clmncre'''' (chancroid) and the discharge from it a small oval 
bacillus has been frequently found either clustered or in chains. It stains readily with 
methj^lene blue, although it easil}^ loses the color. It usually occurs with other micro- 
organisms, and has been found, though not usualljs in the buboes, often occurring with 
the sore. It has not jqX been obtained in pure culture, so that inoculation experiments 
indicating its pathogenicity are not wholly conclusive. 



ANTHRAX. (Splenic Fever; Malignant Pustule; Charbon ; Carbuncle.) 

This disease, which is much more common in the lower animals, 
especially the herbivora, than in man, is widely prevalent in Europe. 
It is comparatively rare in the United States, but in certain regions is 
more common than formerly. 

It is induced in man by accidental inoculation with the Bacillus an- 
thracis, which also incites the disease in the lower animals. Inoculation 




Fig. 99.— a xthrax— Malign ant Pustule— of the Skin. 
From a man who had been handling foreign hides in New York. Bacilli stained, 

may occur through the skin by the agency of flies and other insects 
which have been feeding on animals infected with this disease, through 
abrasions or slight wounds on the hands of those handling their carcasses 
or hides, or in other waj^s. Follow ing this skin inoculation a pustule is 
apt to develop — "malignant pustule'' — and varying iDhases of an acute 
exudative inflammation, which may be hfemorrhagic, sero -fibrinous, 
purulent, or necrotic, accomi)any the local proliferation of the germs 
(Fig. 99). Anthrax bacilli in large numbers maj- be present in the local 



198 



THE INFECTIOUS DISEASES. 



lesion. From this local source a general infection may ensue. General 
infection may occur without evident external lesion. 

Infection with anthrax may occur through the lungs, most often 
among those who handle infected wool or hides, the dust from which is 
inhaled ('^ wool -sorter's disease^'). Under these conditions there may 
be oedema, lobular pneumonia with involvement of the pleura, media- 
stinum, and other adjacent structures. Infection through the gastro- 
intestinal canal takes place by the ingestion of food containing anthrax 
spores, and is apt to be accompanied with inflammatory and necrotic 
changes, which are described in detail among lesions of the intestine. 

When general anthrax infection occurs the post-mortem appearances 
vary. 

Decomposition, as is usual in acute infections, generally sets in early. 
The blood is frequently not much coagulated and dark in color. Haem- 
orrhages and ecchymoses are frequently found in the serous and mucous 
membranes and in various other parts of the body. 

The lungs may show small haemorrhages and oedema, and the bronchi 
may be deeply congested. The x)leural cavities may contain serum. 
The intestines may exhibit the lesions of the so-called intestinal mycosis. 




Fig. 



100.— Bacillus Axthracis Growing ix the Blood-Vessels of the Liter of a Mouse Inocu- 
lated WITH A Pure Culture of the Bacillus. 



The bronchial and other lymph-nodes may be swollen. The spleen may 
be swollen, very dark in color, and soft, sometimes almost diffluent. 

The bacillus may be found, usually in large numbers, in the spleen 
and in the capillary blood-vessels, especially in the liver (see Fig. 100), 
lungs, kidneys, and intestine. 

Cliaracters of the Bacillus Anthracis. 

The Bacillus anthracis is from 5 to 20 ju long and about 1 /ll broad, and is often un- 
even along the sides. The ends of the bacilli are not rounded but square or slightly 
concave, and the bacilli often hang together end to end, forming thread-like structures 



THE INFECTIOUS DISEASES. 199 

(Fig. 101). While the bacilli in the vegetative condition are easily killed, thej' de- 
velop spores outside of the body only, and these are very invulnerable to the action of 
the ordinary germicidal agents and to heat, resisting often for many days the action of 
from two to five-per-cent carbolic acid and defying for 
some minutes the action of live steam. Anthrax bacilli 
are immobile, sometimes capsulated, and are easily 



stained by the anilin dyes. They grow readily on arti- A ^♦^ n ■■ ' 



Kl 



ficial culture media at ordinary room temperatures, tluid- ^^^Xi Q ^^ <^ 

ifying gelatin and usually growing out, before they do ^^ y^^^ 

so, in a network of delicate filaments into the solid me- ^^^^ ^ 




dium. .^^ """^ ▼^ 

Subcutaneous inoculation of cultures of the anthrax 
bacillus into various species of animals induces charac- fig. 101.— Bacillus Anthracis 
teristic lesions. White mice and guinea-pigs are espe- Containing Spores. 

cially susceptible, usually succumbing to the anthrax From a culture, 

septicaemia in from two to four days. Serous exuda- 
tions, often bloody and with many bacilli, develop at the seat of inoculation, while in the 
blood multitudes of the bacilli are found. 

If cultures of the anthrax bacillus be made at a temperature of about 42" C. 
growth occurs, but it is meagre. Spores are not formed as they are at body tem- 
perature, and the virulence of the germ diminishes day by day, so that at last the 
most susceptible animals are not affected by large inoculations of the living organ- 
isms. If fresh cultures of these organisms be made in various stages of their 
diminishing virulence and maintained at their optimum temperature, spores will 
again form, the growth wull become vigorous, and in morphology quite character- 
istic; but the physiological qualities which determine virulence will remain more 
or less in abeyance. 

By inoculation of animals with anthrax cultures, beginning with those which had 
been maintained at 42' C. for from fifteen to twenty days, and thus possessed but feeble 
virulence, and passing to those cultivated at 42° C. for a shorter time and which were 
therefore more virulent, Pasteur was able to secure immunity from anthrax in a series 
of the lower animals (see page 170). Based upon these experiments a method of pro- 
tective inoculation has been practised on a large scale among sheep and other animals 
in some parts of Europe which has been of great economic value. According to some 
authorities the death rate from anthrax has under these preventive inoculations been 
reduced in sheep from ten per cent to about nine-tenths of one per cent, and in cattle 
from five per cent to less than four-tenths of one per cent. 



ACTINOMYCOSIS. 

This disease, which is of occasional occurrence in man, but is more 
common in the domestic animals, especially in cattle and in horses, is 
most frequently characterized by a slow suppurative and proliferative 
process, often leading to the formation of large fungous masses which 
may become calcareous. 

In cattle the new-formed tissue, which develops with especial fre- 
quency in the jaw, is apt to extend beyond the original site and to 
slough, so that not only may the tissues of the tongue, pharynx, larynx, 
etc., be involved, but secondary nodules of similar character may form 
in the lungs, gastro -intestinal tract, and skin. 

In man suppuration with necrosis and the formation of abscesses, 
ulcers, and tistulte, are the most marked lesions in parts near the surface 
of the body. In the Jungs the lesions may be essentially those of an 



200 



THE INFECTIOUS DISEASES. 



acute general bronchitis or in the form of broncho -pneumonia (Fig. 
102), with the formation of new tissue.' 

Abscesses and cavities may form which extend into adjacent parts. 
In intestinal actinomycosis nodular masses of new tissue with ulceration 
may develop in the mucosa and submucosa. Metastases have been de- 
scribed. The excitant of this disease — now most commonly called Strep- 
totlirix actinomyces or Actinomyces bo vis — is a micro-organism which 




Fig. 103.— Actinomyces Growing in Human Bronchus. (The bulbed ends of the fllaments are seen in 

the borders of the colony.) 

The bronchus, cut lengthwise, Is filled with a purulent exudate and its wall is becoming involved. 



seems to be more closely related to the moulds than to the bacteria. It 
is, however, considered here because its botanical position is not yet 
clearly established, and it is still commonly regarded as one of the so- 
called pleomorphous or ''higher bacteria'^ (see page 142). 

The organism often grows in the tissues in the form of little rounded 
masses from a size so small as to be invisible to that of a pin's head. 
They may be transparent or grayish-white or yellow or dark in color. 
Under the microscope these masses often appear in the form of a dense 
group of radiating filaments with more or less bulbous ends ; hence the 
common name ''ray fungus. '^ 

^ For a detailed description of the lung lesions in actinomycosis, with general bib- 
liography, see Hodervpyl, " Actinomyosis of the Lung," New York Medical Record, De- 
cember 13th, 1890. 



THE INFECTIOUS DISEASES. 201 



Characters of Actinomyces. 

The organism may be grown on artificial culture media, flourishing best at body 
temperature. It at first develops in the form of delicate, branching threads, the older 
cultures showing segments which resemble bacilli and cocci, and various bulbous, flask- 
like or club-shaped forms which maj' be the result of degeneration (" involution " forms). 
Successful inoculations of cultures have been made in animals. 

The organism is usuallj^ convej'ed from one animal to another b}" inoculation or by 
contact of the growth with a wound or an abrasion of the mucous membrane.^ 

In the examination of sputum, faeces, pus, etc., for the presence of actinomyces, 
the naked-eye appearances may be of value, since the yellowish-white granules are often 
quite visible, especially on a black background. Suspicious masses may be teased and 
studied unstained, or stained by Gram's method. Sections of tissue containing actino- 
myces may be hardened in alcohol, and sections stained by Gram's method with contrast 
eosin stain. 

Other Organisms Resembling Actinomyces. 

Many forms of micro-organisms of similar general characters to the Streptothrix 
actinomyces have been described, some occurring in connection with infective processes 
in men and the lower animals of which they seem to be the excitants, others living as 
saprophytes in A'-arious situations. Among the apparently pathogenic forms Ave may 
mention the following: 

Streptothrix MaclurcB which is found in connection with a disease commonly called 
mycetoma or " Madura foot, " frequent in the tropics and characterized by new nodular 
groAvths associated with suppuration and necrosis most often affecting the foot.'^ 

Another form has been described in connection Avith a peculiar form of erysipela- 
tous inflammation of the skin; another in the so-called /«?'cm de bcnuf, a disease of cat- 
tle in Guadeloupe. 

Several times organisms of this general character, but differing considerably from 
S. actinomyces, have been found in inflammatory and necrotic lesions of the lungs. 
Whether these are variants of that species or independent species, and how many such 
there are it is impossible at present to say.^ 

Pharyngo-Mycosis Leptothrica. 

Certain filamentous micro-organisms called Lejjtothrix, whose botanical affiliations 
are not yet clear, are of common occurrence in the mouths of healthy persons. Occa- 
sionall}". however, a persistently recurrent attack of " sore throat," with local tenderness 
and sometimes cough and fever, is associated with the groAvth of masses of leptothrix 
in the crj'pts of the tonsils, at the base of the tongue, on the walls of the pharynx, or 
in the nose or superior portion of the oesophagus. The leptothrix masses or colonies 
form thick Avhitish pellicles or patches which may be superficial, or in the tonsils may 
extend deep into the crypts. These masses are usually firmly adherent, often leave 
bleeding surfaces when removed, and the growth is apt persistently to recur. 

Microscopic examination of removed portions of the growth show tufts and bun- 
dles of the thread-like micro-organisms, growing among or directly out from flat epi- 
thelial cell masses and mingled with various other forms of micro-organisms, mostly 
cocci and short bacilli. There maybe overgrowth of epithelium and collections of leu- 

1 For recent bibliographA" of actinomycosis see ScTilegel in Lubarsch and Osterta2:'s 
"Ergebnisse," Jahrg. 5 for 1898. p. 403. 

2 Consult Wright, Journ. Exp. Med., vol. iii., p. 421, Bibl. 

2 For a description of tAvo such cases, with a selected bibliography, see Korris and 
Larkin, Journal of Experimental Medicine, vol. v., p. 155, 1900. 

For a critical summary of this group of organisms, with a full bibliography, see 
monograph by Lachner- Sandoval, "Ueber Strahlenpilze," Strasburg, 1898. 

For full treatment and bibliography, consult the monograph on "L'Actinomycose 
humaine," Poncet and Berard, Paris, 1898. 



202 THE INFECTIOUS DISEASES. 

oocytes in and about the leptotlirix masses. In sections of the tissue or in teased frag- 
ments treated with iodin (LugoTs solution) the leptothrix threads are readily differen- 
tiated from the tissue elements and from other micro-organisms, by their dark color. ^ 



INFLUENZA. (Epidemic Catarrhal Fever ; La Grippe.) 

This is an infectious disease characterized by fever, physical and 
mental prostration, and exudative iniianimations in different parts of the 
body. Thus there may be exudative inflammation in the respiratory, 
digestive, and nervous systems, either singly or together. Sometimes, 
however, these local inflammations may be absent when the disease may 
be marked by the characteristic prostration and symptoms of toxaemia, 
^one of the lesions appear to be characteristic. The inflammation of 
the lungs is usually of the broncho -pneumonic type and is apt to involve 
the interstitial tissue, presenting the characters of the so-called ^^ purulent 
infiltration. " 

The numerous bacterial studies which up to 1892 had been made on 
epidemic influenza had failed to reveal any micro-organism which could 
fairly be regarded as of etiological significance, although some of the 
complicating inflammations of the lungs had been shown to be very fre- 
quently associated with the pyogenic cocci — Staphylococcus pyogenes 
and Streptococcus pyogenes and the Dijilococcus pneumonise.^ 

Early in 1892 Pfeiffer, Kitasato, and Canon' described the occurrence 
in the bronchial exudate and in the blood of influenza patients of a very 
small bacillus, hitherto unknown or possibly noted earlier by Babes. 
This bacillus — B. infliienzce — was sometimes present in the bronchial exu- 
date in enormous numbers, and often with little or no contamination 
with other germs. It was found at the seat of other local lesions, and the 
pus cells often contained many bacilli. In the blood it was occasionally 
I)resent. It has been found to persist in the body long after the active 
processes have ceased. 

Characters of the Influenza Bacillus. 

The influenza bacillus stains with some difficulty with the simple anilin dyes ; but 
by Ziehl's solution (page 223), or by warmed Loftler's methylene blue (page 151), it is 
readily colored. It does not retain the stain well by Gram's method. The bacilli are 
slender and short (one to one and a half times as long as broad) with rounded ends, 
sometimes lie singly, sometimes in pairs or short chains or heaps, do not form spores 
and are not motile. The organism apparently dies after a few hours' drying in the air 
and soon in water. 

This bacillus grows best at body temperature, on glycerin-agar whose surface has 
been smeared with blood — human, rabbit, or pigeon. It forms very small, scarcely vis- 
ble dcAvdrop-like colonies, which, although growing close together, do not tend to coal- 
esce, as many micro-organisms do. It does not grow at a temperature at which the 
nutrient gelatin remains solid. In beef tea it forms a scanty, cloudy growth. It has 

^ For further details and bibliography, consult Ccmvphell, Medical News, April 
4th, 1896. 

2 Consult Finkler, "Die acuten Lungenentzundungen," 1891, p. 452. 

2 Deutsche medicinische Wochenschrift, January 14th and May 26th, 1892. 



THE INFECTIOUS DISEASES. 203 

been cultivated tlirougli several generations, but usually dies soon. Animal inocula- 
tions have given diverse and not verj^ marked results. 

The earlier observations have been in general confirmed by later studies of others. 

The evideuce that the organism described above is the excitant of 
influenza rests largely ui3on its apparently constant presence, especially 
in the exudates. Its effects in the body are most commonly induced 
through its toxins. That the organism should have been occasionally 
found under other conditions^ does not at all militate against its signifi- 
cance in inciting the manifestations of influenza, since many parallel in- 
stances are known in other infectious diseases. The frequent discrep- 
ancy between the clinical and bacterial diagnosis in influenza is largely 
due to its varying and often obscure clinical manifestations which render 
possible and convenient the use of the name for many phases of catarrhal 
and other forms of inflammation. 

Other Organisms of the Influenza Bacillus Group. 

There are several organisms in the influenza bacillus group which considerably re- 
semble it, some of which appear to be pathogenic, others not so. Thus several ob- 
servers have found in exudates from various sources, but especially in the respiratory 
passages, small immobile asporogenous bacilli growing best under conditions similar 
to those favorable to the influenza germ, the colonies being similar. They are some- 
what larger than the influenza bacillus, and tend to form threads. This organism has 
been called the pseudo-influenza bacillus — B. i^seudo-influenzcB. Its pathogenic capaci- 
ties are not clear, but it evidently differs in this respect from the genuine influenza ba- 
cillus. In stained specimens of exudate the pseudo-bacillus may be mistaken for its 
•relative. 

Another bacillus of this group, B. conjunctimtidis, has been found in conjunctival 
catarrh by several observers in various countries. 



TYPHOID FEVER. 

Typhoid fever is an acute infectious disease incited by the Bacillus 
typhosus. The reaction of the body to this bacillus is usually mani- 
fested by characteristic lesions, especially by hyperplasia and necrosis 
in the lymphatic structures of the intestines and the mesenteric lymph 
nodes, and in the si)leen, as well as by the more general alterations inci- 
dent to toxaemia and septicaemia ; but the infection is occasionally of the 
septicaemic type without characteristic local lesions either in the intes- 
tines, or mesenteric nodes, or other viscera. 

The Bacillus of Typhoid Fever. 

The presence of a bacillus, called Bacillus typhosus, in various parts 
of the body in tj^phoid fever, in a considerable i)roportion of the cases 
examined, has been well established by a large number of observers. 
This bacillus does not occur in the body, so far as is known, except in 
connection with this disease. 

^ See Park, ''Bacteriology in Medicine and Surgery," p. 326. 



204 THE INFECTIOUS DISEASES. 



Characters of the Bacillus Typhosus. 

The typhoid bacillus is usually about three times as long as broad, being about one- 
third as long as the diameter of a red blood cell. It is rounded at the ends, motile, 
aerobic, facultative anaerobic, and asporogenous. It grows readily at room tempera- 
ture on the ordinary media. In cultures the bacilli often 
jA^^^TJt^ cling together end to end, forming threads (Fig. 108). 

/•*9j^/^^\N^ During artificial culture in nutrient broth a poisonous 

^^"^v/ZjiS/r albuminoid product or products are formed which have 

been named typJwtoxin. Injection of this into the rabbit 
FIG. 103.-BACILLUS TYPHOSUS. ^^^^ ^^ addition to general toxic symptoms induce hyper- 
plasia of the intestinal Ivmph nodes. 
From a gelatin culture. Inoculations of the typhoid bacillus into animals, 

while not producing a disease in all respects like that in 
the human subject, may cause death with symptoms and lesions as closely resembling 
those in man as we are often able to produce in animal experimentation. Although 
similar effects may be induced in animals hy inoculation with other germs, the evi- 
dence that typhoid fever in man is produced by the typhoid bacillus, and by this alone, 
is altogether so strong as practically to amount to a demonstration. 

It is probable that the more characteristic symptoms and lesions of 
typhoid fever are largely due to the absorption of toxic snbstances which 
are prodnced as the result of the life processes of the bacteria at the 
point of their greatest accumulation and activity. It should, however, 
be borne in mind that the typhoid bacillus, as is the case with many 
other bacteria, may induce local changes by means of its proteid constit- 
uents which are set free as the organisms disintegrate after their death 
in the body. 

Primary Gharacteeistic Lesioxs. 

We shall first consider the lesions which are most common and char- 
acteristic of typhoid fever. 

The Intestines. — The lesions of the intestines consist of an inflamma- 
tory enlargement (hyperplasia) of the solitary lymph-nodules and of the 
agminated lymph-nodules (Peyer's patches). Necrosis of the nodules 
with ulceration frequentlj^ follows the hyperplasia. 

The process appears to begin with a catarrhal inflammation of the 
mucous membrane, accompanied or immediately followed by changes in 
the lymj)h- nodules. The lesions in the lymph -nodules begin early ; they 
have been observed in jDcrsonswho have died forty-seven hours after the 
commencement of the disease. The increase in size of the agminated and 
solitary nodules may be rapid or gradual. The nodules may be only 
slightly enlarged, or may project far into the lumen of the intestine. 
The enlargement is usually more marked in the agminated than in the 
solitary nodules. Usually the whole of a Peyer's patch is enlarged, but 
sometimes only a part of it. If the enlargement be gradual the different 
nodules which make up a Peyer's i)atch may enlarge, while the septa 
between them remain but little changed, thus giving the patch an uneven 
appearance- 

The patches which are only moderately enlarged are of reddish or 



THE INFECTIOUS DISEASES. 205 

reddish-gray color, are soft and spongy, and their edges blend gradually 
with the adjoining mucous membrane. The patches which are more 
markedly affected are of grayish color, of firm consistence, and rise 
abruptly from the surrounding mucous membrane (Fig. 104) or even 
overhang it like a mushroom. The largest patches are sometimes more 
than three-eighths of an inch thick. 

The enlargement and infiltration may spread from the patches to 
the surrounding mucous membrane, so that the i^atches apx^ear very 
large ; a number of them may become fused together, and there may even 
be an annular infiltration entirely around the lower end of the ileum. 
The infiltration, limited at first to Peyer's patches, may extend outward 
into the muscular coat, and appear in the x)eritoneal coat as small, gray, 
rounded nodules. This condition is usually found only with a few 
patches in the lower end of the ileum; sometimes in the caecum and 
appendix vermif ormis. 

The solitary nodules are affected in the same way as Peyer's x)atches. 
They may be hardly enlarged at all, or be quite prominent, or may be 




Fig. 104. -Hyperplasia of Peyer's Patches Ix\ Typhoid Fever. 

affected over a larger portion of the intestine than are the patches. 
Very rarely the solitary nodules are enlarged, while the patches are not 
at all or but slightly affected. 

The inflammation and enlargement of the agminated and solitary 
nodules may be followed by a healing process. The character of this 
process varies according to the intensity of the previous inflammation. 

If the reaction be slight and the enlargement of the nodules moderate, 
the enlargement gradually disappears, and they resume their normal 
appearance (resolution). In moderate enlargements of Peyer's patches 
resolution proceeds first in the nodules, leaving the septa between them 
for a time still swollen and prominent. This gives to the surface of a 
patch a reticulated appearance. After a time, however, the entire patch 
becomes flattened and uniform. On the other hand, the solitary nodules 
or the separate nodules of a patch may soften, break down, and their 
contents are discharged with some attendant haemorrhage. This leaves 
a bluish-gray pigmentation, due to altered haemoglobin, in the situation 
of each nodule, and this may remain for years. 



206 



THE IXFECTIOUS DISEASES. 



In more severe types of the disease the enlargement of the nodules and 
Peyer's patches ends in ulceration. This takes place in two ways: 

(a) The enlarged nodules or patches become necrotic, soften, break 
down, and discharge into the intestine. In this way are formed small 

ulcers (Fig. 105). These ulcers in- 




crease in size by the same softening 
process, which gradually extends at 
their edges, and in this way ulcers of 
large size may be formed.' The 
ulcers may extend outward to the 
muscularis or to the peritoneal coat, 
or they may involve the peritoneal 
coat also and perforate. 

(b) In the severest forms of the 
disease considerable portions of the 
enlarged i)atches may slough and 
become detached, leaving large ulcers with thick, overhanging edges 
(Fig. 106). The slough may involve only the nodules, or it may involve 
also the muscular and peritoneal coats and perforation may occur. 
These ulcers also may afterward increase in size, and several of them 
may be joined together. When the ulceration leads to perforation, peri- 
tonitis and death are the usual result. In rare cases, however, the 
patient recovers and the perforation is closed by adhesions. 

If the patient recover, the ulcers are covered by granulation tissue, 
their edges become flattened, the granulation tissue becomes firmer and 



Fig. 1U5. -Hypeuplasia op Peyer's Patch in 
Typhoid Fkver with Small Ulcers. 

The separate small ulcers are extending and 
have in part coalesced. 




Fig. 106.— Ulceration of Pey'er's Patches axd Solitary Lymph Nodules in Typhoid Fever. 

The swollen patches and nodules are necrotic except at their edges, the central portions forming a 

ragged slough. 

denser, and this new connective tissue is gradually covered with cylin- 
drical epithelium. 

The minute changes which take place in the development of the in- 
testinal lesion are as follows : 

^ Owing to the frequent involvement of Peyer's patches, the larger intestinal ulcers 
in typhoid fever are apt to have their longest diameter lengthwise "of the gut in con- 
trast to spreading tuberculous ulcers, which, owing to the extension of the local inflam- 
mation along the encircling lymph channels, are apt to have the longest diameter 
crossing the gut. But exceptions to this general rule are common. 



THE INFECTIOUS DISEASES. 207 

At first the blood-vessels around the nodules are dilated and con- 
gested, while the nodules are swollen and the epithelium may fall off. 
Then the nodules increase in size, largely from a growth of new cells. 

This cell growth is essentially an hyperplasia of normal elements of 
the lymphatic tissue, namely, the lymx)h cells and the endothelium of the 
trabeculge and sinuses. There are thus two m.ain types among the new- 
formed cells, first, small cells with relatively large and deeply staining 



A %^'^i 









Fig. 107.— Exdothelial Cells ix Hyperplasia of Peter's Patch in Typhoid Feter. 

These exfoliated and newly formed cells contain various foreign substances— leucocytes, red blood cells, 
fragments of nuclei, etc. Some of them are necrotic and are degenerating. A mitotic figure is seen in one. 

nuclei; and second, larger polyhedral or rounded cells with more or 
less vesicular nuclei. The larger cells may contain foreign substances, 
such as red blood cells or leucocytes (Fig. 107). The occurrence of 
mitotic figures in the endothelial cells while these are in situ, and the 
position and grouping of the large cells apx)ear to prove their endothelial 
origin. The production of new cells is not confined to the nodules, but 
extends also to the adjacent mucous membrane. In many cases also little 
foci of similar new-formed cells are found in the muscular, subserous, and 
serous coats. 

In this stage resolution may take place ; then the new-formed cells 
degenerate and gradually disappear. In severer forms of the disease 
necrotic changes are apt to supervene, leading to the larger and small 
ulcers above described. The factors which determine the death of the 
hyperplastic tissues are not yet fully understood. It is believed by some 
to be directly due to toxic substances formed by the typhoid bacilli which 
kill the tissue cells ; others are inclined to attribute it to the pressure 
which the new-formed cells exert on the nutritive blood-vessels. The 
conclusions on this point which Mallory draws from a long and interest- 
ing series of studies would indicate that a proliferation of the endothe- 
lial cells of the blood-vessels may lead to their occlusion. This observer 
describes the formation of occluding thrombi in the lymph vessels and 
smaller veins. These are composed of the proliferated endothelial cells 



208 THE INFECTIOUS DISEASES. 

which have degenerated, together with iibrin whose formation these 
degenerating cells indnce. The accnmnlation of serons and fibrinous 
exudate about these thrombi and the necrosis of tissue which may now 
ensue, may soon be followed by necrosis of the superficial epithelium 
and the development of ulcers. The accumulation of polymorpho- 
nuclear leucocytes may, according to Mallory, now occur, and, in cases 
which go on to recovery, healing follows by the formation in the usual 
way of granulation tissue with the ultimate restitution of the surface 
epithelium. Mallory lays great stress upon the phagocytic nature of 
the new-formed cells of the veins and lymph vessels. For the signifi- 
cance of this process and other interesting details we refer to the original 
paper. ' 

The lesions which we have described are found most frequently and 
are most pronounced in the lower part of the ileum. They are not 
always, however, confined to this situation. Enlarged and ulcerated 
nodules may be found over the entire length of the ileum and even in 
the jejunum. They may also extend downward and be found in the 
colon, even as far down as the rectum. Similar changes may take place 
in the appendix vermiformis. 

Mesenteric Lymph-Nodes. — The mesenteric nodes undergo changes simi- 
lar to those in the nodules of the intestines, and are usually affected in 
a degree corresponding to the intensity of the intestinal lesion. 

The nodes are at first congested and succulent ; then there is a pro- 
duction of lymphoid cells and large cells as in the intestinal nodules, and 
the node becomes enlarged. When the enlargement has reached its full 
extent, congestion diminishes, and the cells begin to degenerate. The 
degeneration may take place slowly, and then the node gradually re- 
turns to its normal condition ; or more rapidly, and then little foci of 
necrotic, purulent material are formed. If the patient recover the small 
foci are absorbed, leaving a fibrous cicatrix ; the larger foci may become 
dry, necrotic, and enclosed in a fibrous capsule. Intense exudative in- 
flammation may occur in the nodes, which may be densely infiltrated 
with serum, fibrin, and pus. 

The Spleen. — In nearly every case of typhoid fever the spleen is en- 
larged. This enlargement begins, as a rule, soon after the commence- 
ment of the disease, increases rai^idly until the third week, remains 
stationary for a few days, and then diminishes. The organ is congested, 
of dark -red color, and of firm consistence while it is increasing in size. 
After it has reached its maximum size, its consistence becomes soft, and 
there is a considerable deposit of brown pigment. The enlargement ap- 
pears to be due to congestion and hyperplasia. 

Mallory describes proliferation of endothelial cells, especially in the 
blood-vessels and pulp spaces, and the formation of venous thrombi. 

In rare cases the softened spleen ruptures, with an extravasation of 
blood into the peritoneal cavity. There may be infarctions of the spleen, 
which sometimes soften and may apparently lead to peritonitis. 
^Mallory, Journal of Experimental Medicine, vol. iii., p. 611, 1898. 



THE INFECTIOrS DISEASES. 



209 









The Liver. — The liver may present no apparent lesion. It is, how- 
ever, freqnently large, pale, and flabby, and in this condition the liver 
cells may be the seat of simple al- 
bnmmons degeneration. ' - • :' -' ' ^ - » ^ 

Less f recpiently there are present , , , ^ ,'','- V 

in the liver verj^ small, soft, gray- - ^vu'.vr'\ '/ ^ *.-/•»' 

ish nodules (Fig. 108). These focal 
lesions are sometimes too small to 
be distinguished by the naked eye. 
They may be situated about the 
branches of the portal vein or within 
the lobule. Some of these nodules 
consist of masses of small spheroidal 
cells, which may form a diffuse in- 
filtration along the small veins. 
Mallory distinguishes two distinct 
varieties of these focal lesions: one formed in the lymph spaces and 
vessels in the capsule of Glisson by a proliferation of the endothelium 
(Fig. 109) ; the other due to obstruction of liver capillaries, in part by 
the proliferation of endothelium on the spot, in part by emboli of 
endothelial cell origin, which are derived through the portal circulation 

KftB 






Fig. 108.— Focal Area of Exdothelial-Cell 
Proliferation in the Liver in Typhoid 
Fever. 




Fig. 109.— Hyperplasia of Endothelium in the Liver in Typhoid Fever. 
This cut shows a more highly magnifled portion of the focal lesion in Fig. 108. 



from the vessels of the spleen and intestine. Necrotic changes may 
develop in and about these focal cell accumulations. 

Simple focal necroses of the liver and of other viscera, due to the 
action of toxic substances in the body fluids, may occur in typhoid fever 
as in many other infectious diseases.' 

^ For fuller details of studies on these focal lesions in typhoid and other infectious 
diseases, consult Mallory, loc. cit. Reed, Johns Hopkins Hospital Reports, vol. v., 1895. 
Flexner, ibid., vol. vi., p. 259, 1897. 
14 



210 THE INFECTIOUS DISEASES. 

While small foci of cell proliferation may be present in the Mdneys 
as well as other viscera, their occurrence is neither so frequent nor so 
characteristic as in the liver. 

In typhoid fever as in other infectious diseases toxsemia maybe mani- 
fested by disturbance in the circulatory, respiratory, and heat-regulating 
mechanism, and in general metabolism as well as by manifest lesions, 
such as albuminous or other degeneration of parenchyma cells through- 
out the body, and alterations leading to leucocytosis. 

Secondary Lesioxs. 

In addition to the more characteristic lesions of typhoid fever which 
we have described, there are several of secondary or complicating nature. 
These are of sufficiently frequent occurrence in the disease to require 
brief mention. They are in X3art due to the direct action of the typhoid 
bacillus or its soluble poisons ; in part, however, are brought about by 
secondary bacterial infections ; but between these it is often, with our 
present knowledge, impossible to distinguish. ' 

The Digestive Organs. — In the intestine there may be gangrene, some- 
times involving the tissues about the ulcers, sometimes apart from 
these. There may be croupous inflammation of the intestinal mucous 
membrane of either the large or small intestine. A slight peritonitis 
sometimes accompanies the intestinal lesion. Severe peritonitis is 
usually due to perforation, less frequently to ulcers which reach the serous 
coat, but do not perforate. \Yhen there is infiltration of the serous coat 
with the new cell growth, described above, peritonitis may be asso- 
ciated with a production of little gray nodules of the same character 
throughout the peritoneum. Infarctions of the spleen, inflammation of 
the ovaries, and perforation of the gall-bladder are sometimes the incit- 
ing factors in peritonitis. 

Haemorrhage from the intestines may be slight and due to the inflam- 
matory swelling and congestion of the mucous membrane ; or it may be 
due to the ulceration of the follicles and opening of the blood-vessels, 
and is then often profuse. 

There may be hyj)erplasia of the tonsils and of the lymphoid tissue at 
the base of the tongue. Gangrenous ulcers of the sides and floor of the 
mouth may be present. Catarrhal and croupous inflammation of the 
pharynx may be associated with superficial or deep ulceration. Inflam- 
mation of the parotid leading to supi3uration is not infrequent. The suh- 
maxiUary gland may be similarly afl'ected. Enlargement and induration 
of the salivary glands and of the xmncreas in typhoid fever have been de- 
scribed and are believed to be due to hyperplasia of the gland cells with 
accumulation of their secretion. This may be followed by degeneration. 

The Circulatory Organs. — The heart in many cases is the seat of albu- 
minous, fatty, or hyalin degeneration, or of pigmentation. Myocarditis, 
endocarditis, and pericarditis are of occasional occurrence. Thrombi 

1 For bibliography of the extra-intestinal lesions induced by the typhoid bacillus 
see Eoioard, Philadelphia Monthly Med. Jour., vol. i., No. 7, p. 402, 1899. 



THE INFECTIOUS DISEASES. 211 

may form upon the valves or in the heart cavities, and detached frag- 
ments of these may be lodged as emboli in various parts of the body. 
The arteries may be the seat of acute inflammation. If this involve the 
intima, an occluding thrombus may be formed which may lead to gan- 
grene of the part supplied by the vessel. Thrombosis of the veins is not 
uncommon, and is especially frequent in the femoral vein late in the 
disease. 

The Respiratory Organs. — The Larynx is frequently the seat of catarrhal 
inflammation, with or without superficial erosions. Less frequently there 
is croupous inflammation, followed in some cases by destructive ulcer- 
ation ; oedema of the glottis occasionally occurs. 

The Lungs. — Catarrhal inflammation of the large bronchi is very com- 
mon. Broncho -pneumonia occurs in two forms. There may be a severe 
inflammation of most of the bronchi of both lungs, with cellular infiltra- 
tion of the walls of the bronchi and zones of i^eribronchitic pneumonia ; 
or there is an intense general bronchitis, with lobules of the lung corre- 
sponding to obstructed bronchi, either colla^Dsed or inflamed, or both. 

From the long-continued recumbent position of the patients, the pos- 
terior portions of the lungs become congested, dense, and unaerated. 
Sometimes, in addition to this, irregular portions of the lungs become 
hepatized. Less frequently there is acute lobar pneumonia. Infarctions 
are not uncommon, and gangrene occasionally occurs, either associated 
with lobular iDueumonia or with infarctions, or as an independent condi- 
tion. Fibrinous pleurisy and empyema are not infrequent. 

The Genito-TJrinary Organs. — The Mdneys are occasionally the seat of 
an acute inflammation. Catarrhal and croupous and nodular inflam- 
mation of the bladder may occur. Haemorrhage and gangrenous inflam- 
mation in the ovaries have been recorded ; the uterus may be involved. ' 
Orchitis may develop during convalescence. 

The Nervous System. — In addition to chromatolytic changes in the gan- 
glion cells which are common to many infectious diseases, "* there may be 
thrombosis of the venous sinuses and obliterating endarteritis. Acute 
meningitis is rare.^ Degeneration and inflammation of the j)eripheral 
nerves may occur. 

Suppurative Inflammation may occur in almost any part of the body 
in typhoid fever. This may be in the form of boils or of deep abscesses. 
Post-pharyngeal suppuration is often one of the most serious of these 
complications. Post-typhoid bone lesions are often important.* 

1 Lartigcm, New York Med. Journal, June 16tli, 1900, bibliography. 

^ For a study of ganglion cells in cases of typhoid fever see NidtoU, Jour, of Exp. 
Med., vol. iv., p. 189, 1899, bibliography. See also Ewing, "Studies on Ganglion 
Cells," Archives of Neurology and Psychopathology, vol. i., p. 263, 1898. 

=^ For bibliography of typhoid meningitis see WentworiJi, Trans, xlm. Pediatric Soc. , 
vol. xi., p. 145, 1899. 

'^Parsons, Johns Hopkins Hospital Reports, vol. v., pp. 417, 1895. 



212 THE INFECTIOUS DISEASES. 



Septicemic Forms of Typhoid Feyer without Characteristic 

Local Lesions. 

Typhoid fever may occur without the characteristic intestinal and 
associated lesions. In this septicfemic tyi^e of the disease there may be 
no demonstrable lesions other than those which are due to the toxae- 
mia. ' On the other hand, inflammatory processes in the viscera — lungs, 
kidney, spleen, etc. — may be dependent on the presence of the typhoid 
bacillus. The lesions in such cases are not, so far as we yet know, char- 
acteristic, and the post-mortem diagnosis depends largely upon the iden- 
tification of the bacillus. ^ 

Distribution of the Typhoid Bacillus in the Body in Typhoid 

Fever. 

In the early stages of the disease the bacillus may be found in the 
lymphatic structures of the intestines and in the mesenteric lymph -nodes 

and the spleen. It may be present in 
lesions involving the bone marrow, kid- 
ney, liver, lungs, pleura, uterus, testicle, 
and skin,^ as well as in the blood." 
Typhoid bacilli have been repeatedly 
found in the urine and in the bile, and 
may persist here long after the establish- 
ment of convalescence." They may be 
found, though not in such abundance as 
was formerly assumed, in the intestinal 
contents after the disease has become well 
established. Their abundance here ap- 
IDcars to depend somewhat upon the de- 

FiG. 110. "Cluster of Typhoid Ba- ^-ij-Ti ,- -r.i 

ciLLi IN THE SPLEEN. gi"©© of intestiiial ulceration. In the ^as- 

cera they are apt to occur in larger and 
smaller masses or clusters (see Fig. 110). The typhoid bacillus may 
be transmitted through the placenta to the foetus. ^ 

Typhoid bacilli may be present alone or in association with other 
germs in the foci of suppuration which so frequently complicate typhoid 

^ Consult in this connection for cases and bibliography, Gldari, Zeitschrift f . Heil- 
kunde, 1897; Lartigau, JSTew York Med. Journal, vol. Ixx., p. 158, 1899; also Johns 
Hopkins Hospital Bulletin, April, 1899 ; OpMlU, New York Med. Journal, May 12th, 
1900. 

'^ For summary of studies on the typhoid bacillus and tj^phoid fever, with bibliog- 
raphy, consult Z>?m&a?-, "Ergebnisse der allg. Aetiologie der Menschen- u. Thierkrank- 
heiten," Jahrg. I., Abth. 1, p. 605, 1896. 

2 See Pratt, Jour. Boston Soc. Med. Sciences, vol. iii., p. 170, 1899. 

'^ ^ee Auerbach, Deutsche med. Wochenschr., December 6th, 1900, Bibliography. 

^ G'Lcyn, Johns Hopkins Hosp. Bull., vol. x., p. 109, 1899; also Curschmann, on 
typhoid cystitis, Munchener med. Wochenschr., October 16th, 1900. 

•^Ref. Lartigau, New York Med. Jour., June 16th, 1900. 




THE IXFECTIOUS DISEASES. 213 

fever, also iu the exudate in inflammations of the serous membranes and 
in the endocardial vegetations. ' 

Some of the inflammatory complications which occur in typhoid fever 
are due to the growth of the h^jCillus in unusual places in the body ; but 
manj^ of them are due to a secondary infection with other germs, notably 
with the pyogenic cocci, ^ also with the colon bacillus and the pneumo- 
coccus. ^ 

Modes of Infection with the Typhoid Bacillus. 

Infection with the typhoid bacillus seems usually to occur through 
the gastro -intestinal canal. In a large proportion of cases the bacilli 
are conveyed by means of food, and especially of milk and drinking- 
water, which have been polluted with the excretions of persons suffering 
from the disease. Many serious epidemics of typhoid fever have been 
traced to pollutions of milk and drinking-water from such sources.* 

Oysters which have been taken from grossly polluted waters, as near 
sewer openings, have been the means of conveying the germs. '" 

In milk the typhoid bacillus not only remains alive for long periods, 
but undergoes active multiplication. It may remain long alive in water 
and even for a time multiply. In the soil and when dried it may remain 
alive for months. Frozen in ice it has been found alive after more than 
three months. It is readily killed by exposure to strong sunlight. 

Preventive Inoculations. 

Preventive inoculations have been practised on a large scale in man 
by the method of Haffkine with ai^parently favorable results. In this 
method cultures of the bacillus are killed by heat and the emulsion is 
injected subcutaneously. 

Agglutination. 

It has been found that if the serum of an animal which has been immunized against 
a motile organism be placed in contact with these organisms in a fluid medium, the or- 
ganisms cease to move and gather into flocculi or clumps. By the use of this phenomenon, 
called agglutination, a method of clinical diagnosis of considerable value has been de- 
vised and especially emploj^ed in typhoid fever, since in this disease a certain degree 
of immunity or at least a certain specific quality in the serum is acquired during an 
attack of the disease. 

The nature of this agglutination, which may occur with dead bacilli also, is not yet 
understood, nor is the reaction altogether limited to the bacterial species which induces 
the tolerance. Furthermore, it appears that agglutination may be induced by various 

^ See Flexner, Journal of Patholog}^ and Bacteriologj^ vol. iii., p. 202, 1895, and 
Johns Hopkins Hospital Reports, vol. v., p. 343; also Mace, "Traite de Bacteriologie," 
1901. 

■^ For full consideration of the pyogenic powers of the typhoid bacillus, consult 
Dmochowski and Janoicski, Ziegler's Beitr. z. path. Anat., etc., Bd. xvii., p. 221, 1895. 

3 Keen, "The Surgical Complications of Typhoid Fever," 1898. Hare, "The Medi- 
cal Complications of Typhoid Fever," 1899. 

■^ Freeman, New York Medical Record, March 28th, 1896, bibliography. 

'"Freeman, Alban}' Med. Annals, vol. xviii., 1897, bibliograph}^; Mosny, Revue 
d'Hygiene, t. xxii., pp'. 12, 102, 198, 1900; Herdman and Bo7/ce, Thompson Yates Labora- 
tory Report, vol. ii., supplement, 1899. 



214 THE INFECTIOUS DISEASES. 

organic and inorganic chemical substances. Finally, it has been shown that if the de- 
fibrinated blood of one animal be injected into an animal of different species, the blood 
of the latter acquires a marked agglutinating power for the red blood cells of the ani- 
mal w^hose serum was originally injected. Thus it appears that the phenomenon of 
agglutination is general and not limited to bacteria. 

Agglutination has been used as a means of diagnosis in other infectious diseases, 
especially in Asiatic cholera. It has been found useful also in the identification of 
species in various forms of bacteria. ^ 

The Typhoid and Colon Bacillus. 

Much difficulty has been encountered in distinguishing betw^een the typhoid bacillus 
and various forms of the colon bacillus when they occur together, as may be the case 
in contaminated water or in the dejecta of persons suffering from typhoid fever. As a 
result of this difficulty, a very close relationship has been assumed between typhoid and 
colon bacilli. This assumption is not wholly justified by the facts, since many of the 
biological as well as some of the morphological characters of the two are quite dissimilar. 

The difficulty in distinction is largely limited to the identification of colonies on the 
common media usually employed in the gelatin and agar plates. Hiss has shown how 
by a slight modification of the common methods the growth of each form is quite char- 
acteristic, so much so that pure cultures may be made from the first mixed plates with- 
out difficulty.'^ When once the two forms are separated, distinguishing characters are 
readily demonstrable. 

Methods of Staining the Typhoid Bacillus. 

The bacilli from artificial cultures stain readily with the ordinary anilin dyes, such 
as fuchsin and methylene blue. In sections, however, they do not stain so readily. 
They are decolorized by Gram. They may be stained by ZiehVs solution (see page 
223). Stain for half an hour, decolorize in alcohol, clear in oil of cedar, mount in bal- 
sam. The decolorization in alcohol should be carefully done to avoid the removal of 
too much color. Flexner recommends the staining in Loffler's methylene blue solution 
for two hours; then put in acetic acid solution 1 : 1,000 for several minutes; dehydrate 
in absolute alcohol: clear and differentiate in oil of cloves; mount in balsam. The aim 
in both of these methods is to leave the nuclei faintly colored, but not so much so as to 
conceal the clusters of more deeply stained bacilli. 



ASIATIC CHOLERA. 

Asiatic cholera is a disease incited by the growth and proliferation in 
the intestines of a slightly curved or spiral -shaped bacterium, which is 
called the cholera spirillum — Spirillum cholerce Asiaticce (Vibrio cholerse 
Asiaticse). This organism in the early and active stages of the disease 
may be present in enormous numbers in the contents of the small intes- 
tine, often penetrating the mucosa. It is usually confined to this situ- 
ation. Its deleterious effects upon the body appear to be largely due to 
the production of toxic substances, which in addition to serious intestinal 
irritation or lesion may on absorption incite those systemic disturbances 
which characterize profound toxaemia. 

^ For further details w^e refer to the special bibliography on the subject, w^hich 
may be found in Mace's "Bacteriologie," 1901, and to works on clinical pathology. 
^M'.ss, Jour. Exp. Med., vol. ii., p. 677, 1897. 



THE INFECTIOUS DISEASES. 215 



Lesions of Asiatic Cholera. 

In some cases of cholera there are no marked changes to be found 
after death, and in no case are the lesions distinctive of this disease. 

If death occur during the invasion of the disease or in the stage of 
collapse, the appearances in the more marked cases may be summarized 
as follows : 

The bodies may remain warm for some time, and the temperature 
may rise for a short time after death. The rigor mortis usually begins 
early and lasts for an exceptionally long time. The muscles sometimes 
exhibit a peculiar spasmodic twitching before the rigor mortis sets in, 
especially the muscles of the hand and arm. 

The Skin is of a dusky gray color ; the lips, eyelids, fingers, and toes 
are of a livid X)uri3le. The ends of the fingers are shrivelled, and the 
cheeks and eyes sunken. 

The Brain. — The sinuses of the dura mater are filled with dark, thick 
blood. The pia mater may be normal, or oedematous, or ecchymotic, 
or infiltrated with fibrin. The brain is usually normal, but may be dry 
and firmer than usual. 

The Lungs are retracted and anaemic, the pleura may be dry or coated 
with fibrin. The Heart is normal. The Peritoneum may be dry or coated 
with a laj'er of fibrin. 

The Stomach is usually unchanged, but may be the seat of catarrhal 
inflammation. The Small Intestine. — There may be ecchymoses in the 
mucous membrane ; the mucous membrane may be soft and oedematous ; 
there may be general congestion, or the congestion may be confined to 
the peripheries of the solitary and agminated nodules, and these nodules 
may be swollen ; or there may be croui30us inflammation and superficial 
necrosis. All these changes are usually most marked at the lower end 
of the small intestine. There is apt to be post-mortem desquamation of 
the epithelium. The characteristic rice-water fluid may be found in the 
intestines after death, or instead of this dark-colored, bloody fluid. The 
Large Intestine is usually normal, but in some epidemics croupous inflam- 
mation occurs in a considerable number of cases. 

The Spleen may be soft. The Liver may show small areas of granular 
or fatty or hyalin degeneration. 

The Kidneys are often increased in size, with white and thickened cor- 
tex and congested pyramids. The epithelium of the cortical tubes may 
contain coarse granules and fat globules, or be necrotic. The tubes 
may contain casts and disintegrated epithelium. The Uterus and Ovaries 
may be congested and contain extra vasated blood. 

If the patient do not die until the stage of reaction, the body does not 
present the same collapsed appearance, and there are often inflammatory 
changes in different parts of the body, especially in the larynx, the lungs, 
the stomach, and the intestines. 



W' 



216 THE INFECTIOUS DISEASES. 



Characters of the Cholera Spirillum. 

The cholera spirillum, which was discovered by Koch in 1883, is a curved rod with 
rounded ends from, 0.8 to 2.0 // long, asporogenous, aerobic, and motile. When growing 
under suitable conditions these rods are apt to cling together by their ends, forming S- 
shaped structures or spirils, often of considerable length (Fig. 111.) The organism stains 
readily and grows abundantly on the ordinary culture media. The life period is short 
and various degenerative " involution " forms are apt to be present in old cultures. It 
grows best at about blood heat; grow^th ceases at about 16° C, but may survive a re- 
duction of the temperature to — 10° C. It is quickly killed 
by drying or by the temperature of boiling water. Acids 
are inimical to its growth. It may retain its vitality for 
a considerable time in water. On moist surfaces, such as 
damp linen, earth, vegetables, or in milk, it may rapidly 
proliferate. 

The results of animal experiments with the cholera 
germ are not in themselves decisive in determining its 
FIG. lll.-Spm^LLTO CHOLERA relationship to this disease, since animals do not react in 

its presence as man does. However, the constant occur- 
From a cu ure. rence of this organism in Asiatic cholera, its absence from 

the body under other conditions, and the accidental labo- 
ratory infections which have several times occurred in men handling pure cultures of 
the germ, leave no doubt as to its significance as the excitant of this disease. 

The infectious organism is usually convej'^ed from one person to another by the 
pollution of food or drink with the discharges which contain the virulent germs. 

It is often of the highest importance to determine, at the earliest possible moment, 
whether or not a suspected case be one of Asiatic cholera or some other form of acute 
intestinal disorder, so that in the former case the proper measures may be instituted to 
prevent the spread of the disease. The characters Mdiicli are developed in cultures of 
the cholera bacillus enable an expert bacteriologist to distinguish this organism from 
all other known forms. But the scope of this work does not permit a detailed descrip- 
tion of the cultural peculiarities of the germ. Kor should the responsibility of such de- 
terminations be assumed without adequate preliminary laboratory experience. By 
taking together the morphological and biological characters, it is possible, usually on the 
second or third day, to determine whether the intestinal contents of a suspected case do 
or do not contain the bacillus of Asiatic cholera. 



Preventive Inoculation, Antitoxic Cholera Serum and its Lysogenic Action. 

A large amount of work has been done, looking toward artificial immunization of 
man against Asiatic cholera in the East and preventive inoculation practised by tlie 
method of Haffkine appears to have given encouraging results. This method consists 
in the subcutaneous injection of cultures of the cholera bacillus; first, those whose viru- 
lence has been diminished, and then, those in which the virulence has been exalted by 
artificial means. 

Pfeiffer has shown that the spirillum of Asiatic cholera, put into the jDeritoneal 
cavity of an artificially immunized guinea-pig, is quickly immobilized, swells, and be- 
comes granular and soon disappears. A similar effect can be secured in tubes h}" a 
mixture of the antitoxic serum and fresh serum to which the spirilla are added. This 
action of the antitoxic serum upon the bacteria is called lysogenic, and its use has been 
proposed as a test, on the one hand, of the specific character of a suspected spirillum; 
and, on the other, with a definitely known spirillum to emplo}" the lysogenic action of 
tlie serum in a suspected case of disease as a diagnostic test. 

This lysogenic action of specific sera, when mixed either with the peritoneal fluid 
within an animal or with normal serum in vitro, is not peculiar to the so-called anti- 



THE INFECTIOUS DISEASES. 217 

cholera serum, but lias been observed in other cases — for example, in typhoid serum with 
the typhoid bacillus. The relationship between the bactericidal action of these anti- 
toxic sera and that of normal sera is not yet clear. 

Other Spirilla Resembling the Cholera Spirillum. 

There are several fairly distinct forms of spirilla, some of which appear to be re- 
lated to the cholera organism, which have been occasionally found in various situations. 
One of these is the so-called Vibrio iproteiis or spirillum of Finkler and Prior. This 
oi'ganism was found by these observers in the dejecta of persons suffering from cholera 
nostras, shortly after the discovery by Koch of the cholera spiiillum, which at first it 
was thought closely to resemble. The cultural characters, however, abundantly suffice 
to differentiate the organisms. The Yibrio proteus is sliglitly pathogenic for certain 
lower animals, but not for man. 

Several forms of spirilla of somewhat similar general characters have been found in 
various situations; thus in cheese, by Denecke, 8. tyrogermm ; in a chicken epidemic 
and in sewage, hj Gamaleia and by Pfuhl, Yibrio Metschnikovi ; in the dejecta during 
a cholera epidemic at Massawah, Vibrio Massawah, etc. Spirillum sjmtigenum, of fre- 
quent occurrence about the teeth and in the saliva of healthy persons, is not pathogenic. 



TUBERCULOSIS. 

Tuberculosis is an infectious disease characterized by inflammatory 
and necrotic processes in the body and incited by the presence and 
growth of the Bacillus tuberculosis (tubercle bacillus). The most dis- 
tinctive morphological feature of tuberculosis is the development under 
the influence of the tubercle bacillus of larger and smaller gray or white 
or yellow, firm or friable masses of tissue called tubercles. 

The effect on the body cells of the presence and growth of the tubercle 
bacillus varies considerably, depending upon the number and virulence 
of the germs i^resent, the character of the tissue in which they lodge, and 
the vulnerability of the individual. In general, it may be said that 
tubercle bacilli may stimulate the connective -tissue cells in their vicinity 
to proliferation ; or they may excite emigration of leucocytes from blood- 
vessels and lead to the production of other exudates ; or they may cause 
death of tissue. Thus the phases of inflammation which are excited by 
the tubercle bacillus are productive, exudative, and necrotic. The tuber- 
cle bacillus may incite these changes separately or simultaneously, in 
the sequence just indicated or in some other; and now one, now another 
of them may preponderate. 

Morphology of the Lesions of Tuberculosis. 

Tuberculosis manifests itself most often in the form of an inflamma- 
tion affecting some one part of the body, as the lungs and bronchial 
lymph-nodes (the parts most frequently involved in adults), the gastro- 
intestinal tract or the skin — "localized tuherculosis.''^ In a considerable 
proportion of cases the local lesions induced by the tubercle bacillus 
are in the form of circumscribed nodules or masses of new-formed cells 
or tissue which are called tubercles, or if small miliary tubercles. ' 

^ ^ The term miliary tubercle, which arose from the coincidence in size between small 
foci of tuberculous inflammation and some forms of millet seed, is now very liberally 



218 THE INFECTIOUS DISEASES. 

Such a localized tuberculosis may retaiu throughout the characters 
of a local inflammation, or it may be accompanied by the clinical 
evidences of systemic infection. It may give rise through metastasis 
to the successive development of tuberculous inflammations in other 
parts of the body, or to a sudden development of small foci of tubercu- 
lous inflammation in many parts of the body at the same time — general 
miliary tuberculosis. 

A general infection may occur by the difl'usion through the body of 
bacilli derived from a local tuberculosis, such as tuberculous phlebitis or 
arteritis, tuberculous inflammation of the thoracic duct, or from the 
breaking into a vessel of a tuberculous lymph node. It is probably 
seldom that a sufficient number of tubercle bacilli enter the blood chan- 
nels at once to account for the enormous number of tubercles which are 
sometimes found in acute general miliary tuberculosis ; but it is not un- 
likely that from the earliest formed tubercles which develop in the walls 
of the smaller blood-vessels new distributions of bacilli may speedily 
take i3lace.' 

In many cases, however, the lesion is not focal or circumscribed but 
diffuse, and more or less widely infiltrates or replaces the tissues in- 
volved. This is called diffuse tuberculous inflammation. 

Miliary Tubercles. — Miliary tubercles are small nodules of irregular 
shapes (Plates IV., YI., and VII.), the smallest hardly visible to the 
naked eye. The smaller tubercles are gray and translucent ; the larger 
are usually, especially in the central parts, opaque and white or yellow 
on account of the necrosis which is apt to commence here. 

In studying the reaction of the living tissues to the tubercle bacillus 
it should be always borne in mind that while, as a Avhole, the lesions 
produced are quite characteristic, there is still no one structural feature 
or combination of features of tubercles or tuberculous inflammation which 
is absolutely distinctive of the action of this bacillus. In doubtful cases 
the demonstration of the presence of the germ itself may be necessary for 
the establishment of the character of the lesion.^ 

The experimental studies in animals, as well as the morphological 
data gathered from the examination of tuberculosis in man, show that 

applied to tubercles which are very much larger as well as to those which are very 
much smaller than millet seeds. It is convenient to designate a small mass of new 
tissue formed under the influence of the tubercle bacillus, whatever its minute struc- 
ture, as a tubercle granulum (see Fig. 112). Very frequently two or more tubercle 
granula are joined together by a more diffuse formation of tubercle tissue to form larger 
or smaller miliary tubercles — conglomerate tubercles (see Fig. 113). 

^ It is well in the endeavor to understand the occurrence of general miliary tuber- 
culosis or of the less striking instances of distribution of the bacilli that two varying 
factors are constantly active and significant ; first, the virulence of the bacilli, which may 
be slight or extreme; and, second, the vulnerability of the infected individual— ^■.^., his 
" predisposition " — which also may be slight or extreme. Thus the distribution of 
bacilli, be these few or many, from an infective focus, may be in different individuals 
or at different times in the same individual of quite different significance. 

For a critical resume of the etiology and mode of origin of miliary tubercles, with 
bibliography, see Benda, in Lubarsch and Ostertag's "Ergebnisse," Jahrgang v., p. 447. 

^ The term tubercle tissue, which is in common use, indicates a tissue formed under 
the influence of the tubercle iDacillus rather than a tissue which is morphologically chra- 
acteristic of tuberculosis in distinction from other forms of new tissue. 



THE INFECTIOUS DISEASES. 



219 



when tubercle bacilli in moderate numbers lodge and develop in the liv- 
ing body one of the early local effects is a proliferation of the connect! ve- 

tissue and endothelial cells.' These 
^, become larger and polyhedral, with 

'^, ^, i. <j'V ® ^i conspicuous nuclei (Fig. 112). 

f^ ?.^ ^ ';'^ -'^ J*^' A new reticulum or stroma may 

0%5'J ^"''^ '; , ^ ^^^ :^ form hand-in-hand with the growth of 

" ./' * ^^ ^ , these new cells, or the old stroma may 

" f ' . ^ . " ' • * f persist, adapting itself in form and 



^ 



arrangement to the new conditions. 



Either after the connective-tissue 
cell proliferation or hand-in-hand with 
it, or preceding it, or altogether inde- 
pendently of it, emigration of leuco- 
cytes and extravasation of serum may 
take place from blood-vessels in the 
vicinity of the germs. During the 
more or less active cell x>roliferation 
which occurs under the influence of 
the tubercle bacillus multinuclear cells 
— giant cells — may be formed (Fig. 113), either by persistent nuclear 
division in growing protoplasmic masses which do not divide into sepa- 
rate cells, or by the coalescence of the bodies of cells already formed. 






Fig. 112.— a Small Miliary Tubercle. 

This is growing in the liver ; is composed 
mostly of new-formed polyhedral cells closely 
packed with little intercellular stroma. At 
the centre coagulation necrosis is commenc- 
ing. 




•;>/• .:v- ■:,■.;, 






cv.; 










Fig. 113.— a Miliary Tubercle with Giant Cells. 

This tubercle is of the conglomerate type, made up of four granula, the larger one showing coagulation 
necrosis in the central portion. From the peritoneum. 

More or less new tissue with numerous small spheroidal mononuclear 
cells and little stroma may form in and about the tuberculous foci. 



^ The studies of Wechsberg indicate that in some cases at least the first effect of the 
tubercle bacillus upon the living tissue is destructive, so that the characteristic cell pro- 
liferation which follows may not be altogether due to a direct formative stimulus to cell 
proliferation furnished by the bacillus. See Wechsbeiy, " Beitrage zur Lehr. v. d. primaren 
Einwirkung des Tuberkelbacillus, " Ziegler's Beitrage zur path. Anat., Bd. xxix., 1901. 



220 



THE INFECTIOUS DISEASES. 



Blood-vessels are not apt to develop under the influence of the tubercle 
bacillus. Old blood-vessels are, on the other hand, usually obliterated 
as the new tissue forms. 

Sooner or later, under the influence of the tubercle bacillus, there is 
usually a damage of cell and tissue, which may lead to coagulation necro- 
sis in the new-formed as well as in the old tissue of the infected region. 
This necrosis is more apt at first to manifest itself in the central portions 
of the tuberculous foci (Fig. 114) and may progress outward; the nuclei 
become fragmented or disappear, or fail to stain in the usual way, the 











.*♦'# 






• (J 


















U^^^^^r/yxt 



Fig. 114.— a Miliary Tubercle in the Lung. 
Shov/ing polyhedral cells, small spheroidal cells, and giant cells, with coagulation necrosis at the centre. 



protoplasm becomes more homogeneous, and cells and stroma form at 
last an irregularly granular mass of tissue detritus which tends to disin- 
tegrate (coagulation necrosis, cheesy degeneration, caseation), forming 
cavities or, if on free surfaces, ulcers. 

As coagulation necrosis progresses, the tubercle masses lose the gray 
translucent appearance which in their early stages they are apt to pre- 
sent to the naked eye and become more opaque and of yellowish -white 
appearance at the centres. 

Finally dense fibrous tissue may form in and about foci of tuberculous 
inflammation, encapsulating or sometimes entirely replacing the more 
characteristic new -formed structures. It is in this way — by the forma- 
tion of connective tissue — that such repair as is possible after local tuber- 
culous inflammation, is brought about (Fig. 259, p. 467). 



THE INFECTIOUS DISEASES. 221 

Before the discovery of the tubercle bacillus and while knowledge of 
the lesions of tuberculosis was largely limited to their morphology, it 
was natural that much stress should be laid upon the variety in structure 
which the nodular growths called tubercles present, and that elaborate 
classifications and groupings of tubercles were often deemed important. 

With an exact knowledge of the excitant of the new growths and of 
the varying j^hases of their development in the body, the morphological 
peculiarities of tubercles are not now to be regarded as of such extreme 
significance, since they for the most part indicate simply variations in the 
local effect of a definite x)oison. These variations are due as we have 
seen to differences in the amount and intensity of the poison, to the degree 
of susceptibility of the individual, to the structure of the particular tissue 
or organ involved, and to the extent and variety of local complications 
caused by other agencies. 

It is, however, usually convenient and sometimes important to recog- 
nize structural tyjDcs in miliary tubercles. Thus they may be composed 
wholly of small spheroidal cells — ^'lymplioid tubercles,''^ or of larger poly- 
hedral cells' ^'poli/hednd-ceUed tubercles, ^^ or of both forms of cells together 
and with or without a new-formed stroma ; or of any of these combina- 
tions with giant cells. Then coagulation necrosis, which may occur in 
tubercles of any type ; development of new dense connective tissue ; as- 
sociation with various phases of simple exudative inflammation — ^all of 
these contribute to the variety in the structural types of miliary tuber- 
cles. 

Diffuse Tuberculous Inflammation (Diffuse Tubercle). — 1. If the infec- 
tion with tubercle bacilli be extensive, or if step by step the bacilli are 
distributed in the tissues about the primary seat of infection, consider- 
able amounts of tubercle tissue of one or other form may develop and 
pass into the condition of coagulation necrosis, so that at length large 
necrotic masses, with a comparatively small amount of well-defined 
tubercle tissue, either diffuse or in the form of granula, may alone re- 
main to indicate the character of old and slowly progressive local infec- 
tion. This form of lesion is found in the large tuberculous masses in the 
brain, in the mucous membrane of the bronchi, in large flat masses on the 
serous membranes, and in the diffuse, cheesy infiltration of the lymph 
nodes, kidneys, ureters, bladder, jDrostate, testicle, and uterus. 

These large areas of tuberculous inflammation are apt to be white or 
yellow in the central and necrotic portions, which are sometimes dense, 
compact, and hard, sometimes soft and friable. These areas are not in- 
frequently surrounded by an irregular gray zone of tubercle tissue or by 
a dense fibrous-tissue capsule. 

2. In marked contrast with the phase of diffuse tuberculous inflam- 
mation just described, though often associated with it, is that in which 
the formation of inflammatory exudates is a i^rominent feature. This 
exudative form of tuberculous inflammation is best exemplified in the 

' Some of these larger cells are regarded by many as so-called " plasma cells " (see 
p. 103). 



222 



THE INFECTIOUS DISEASES. 



luugs by some of the forms of acute phthisis (see page 473). The tuber- 
cle bacillus is under certain conditions markedly pyogenic, and when it 
rapidly develops in the air spaces of the lungs or suddenly gains access 
to them in large quantities pus, serum, fibrin, and exfoliated or prolifer- 
ated epithelial cells may collect in and largely fill the air spaces, and then 
the whole new exudate and the old lung tissue may, over larger or smaller 
areas, rapidly undergo coagulation necrosis. (Plates VIII. and X. ) 

Thus in one phase of tuberculous inflammation the intensity and 
rapidity of the local poisoning by the bacillus do not permit of the 
formation of organized new tissue at all, but only of exudative products 



»^S, 


















Fig. 115.— Exudative Form of Tuberculous Inflammation Showing tubercle Bacilli. 
From the lung of a child. The size of the bacilli has been slightly exaggerated in the cut. 

which are apt soon to become necrotic (Fig. 115). Less intense degrees 
of exudative inflammation are liable to develop in the vicinity of miliary 
tubercles anywhere in the body. 



Characters of the Tubercle Bacillus. 

The bacillus tuberculosis is a long, slender bacterium varying in length from 3 to 
4 ju (from one-quarter to one-half the diameter of a red blood cell) and in breadth from 
0.2 to 0.5 //. It is frequently more or less curved, and the individual bacilli may cling 
together end to end, forming threads or chains. It may occur in branching forms. ' 

The bacillus (Fig. 116) is stained with difficulty by the anihn dyes (see below), and 

^ Branching forms of the tubercle bacillus have been frequently seen, and while 
their significance is not yet altogether clear, the tendency at this time is to separate this 
organism with the diphtheria bacillus and the so-called streptothrix or actinomyces 
forms into a group apart from the bacilli. Whether, as many think, they are more 
closely allied to the moulds than to the bacteria, or whether they should be considered 
in a class by themselves are problems still unsolved. For the present, we may wisely 
consider the tubercle bacillus as one of the bacteria. 

For studies and bibliography on this subject, consult Schulze, Zeitschrift f. Infec- 
tions -Krankheiten, Bd. xxxi., p. 153, 1899; and Lubarsch, ibid., p. 187. 



THE IXFECTIOUS DISEASES. 



223 




riG. 



116.— Tubercle Bacilli ix SpriUM 
Case of Pulmonary Tuberculosis, 



FROM 



ShOTving the bacilli stained with f uchsin and pus cells 
stained for contrast with methylene blue. 



when stained often presents an irregular beaded or knobbed appearance, due to an un- 
evenness in the coloring of the protoplasm, or to involution changes. It is immobile 
and spores have not been demonstrated 
in it. 

At the temperature of the body it 
can be grown on many of the artificial 
culture media. 

The growth of the tubercle bacillus 
in cultures is ver}^ slow in comparison 
with that of most of the pathogenic 
micro-organisms. After several weeks' 
growth it forms dry, scaly masses or 
thin, wrinkled pellicles on the surface 
of the media (Figs. 117 and 118). It 
requires a certain amount of oxygen for 
its growth, and thrives best in the dark. 
It is killed by an exposure of a few 
hours to direct sunlight, or if moist is 
killed by an exposure of from ten to 
fifteen minutes to 70° C. On the other 
hand, it may long retain its vitality in 
the dried condition. 

Cultures can be continued indefi- 
nitely from generation to generation with 
a slowly diminishing virulence which 

finall}^ is largely lost. Under certain conditions the virulence may be restored or en- 
hanced by successive inoculations into susceptible animals. 

The tubercle bacillus does not, so far as we know, grow in nature outside of the 
bodies of men and certain warm-blooded animals. It is thus apparently strictly parasitic. 

Methods of Staining' the Tubercle Bacillus. 

Ix Fluids. — For the examination of fluids, such as sputum, ' etc., the material 
should be spread in a thin layer on a cover glass, dried in the air, and then passed thrice 
through the flame (see page 150). 

While, as has been said above, the tubercle bacillus is stained much less easily with 
the anilin dyes than are most bacteria, it can be deeply colored b}* the use of accessory 
agents which intensify the stains or render the protoplasm of the bacilli more accessible 
to them. Btit when once stained the tubercle bacillus clings with great tenacity to its 
color in the presence of the usual decolorizing agents. 

A variety of methods are in vogue for staining the tubercle bacillus, most of them 
being more or less unessential modifications of the original process formulated by Koch 
and Ehrlich. Ziehl's solution is among the most useful. This is made by adding to a 
five-per-cent aqueous solution of carbolic acid about one-tenth its voltime of saturated 
alcoholic solution of fuchsin. This carbolic fuchsin will keep unchanged for a long time. 

The prepared cover glass is floated in a watch glass or porcelain capsule — specimen 
side down — on this coloring fluid, and gently heated almost to boiliDg for from three to 
five minutes. 

The entire specimen is thus completely stained, tubercle bacilli, tissue elements, and 
other bacteria which may be present, all in the same way. The next step is to remove 
the color with acid from all the structures which may be intermingled with the tubercle 
bacilli; the latter, owing to the tenacity with which they retain the color, being bat 
slightly affected. This is done b}" dipping the cover glass into an aqueous or alcoholic 
solution of five-per-cent sulphuric acid, and shaking it about for a few seconds. Under 



^ It is well in obtaining sputum for examination in cases of suspected pulmonary 
tuberculosis to secure that which has been raised during several hours, including the 
early morning discharge. 



224 



THE INFECTIOUS DISEASES. 



the influence of the acid the specimen on the cover glass loses its red color and becomes 
gray or colorless. It is then thoroughly rinsed in three or four successive portions of 
alcohol, and finally in water. By this manipulation the red color may be to a slight 
extent restored. 

Care should be taken not to expose the specimen too long to the action of the acid, 
because then the bacilli may be also partially or completely decolorized. A little ex- 
perience will enable the experimenter to judge of the proper time for the action of the 





Fig. 117. 



Fig. 117.— Culture of Tubercle Bacillus on Glycerin Agar. 
Fig. 118.— Culture of Tubercle Bacillus on Glycerin Agar. 



Fig. 118. 

-From tuberculosis in man. 
-From tuberculosis in the bird. 



acid. The specimens may be studied in water with the use of an oil immersion lens 
and the Abbe condenser, or they may be dried in the air and mounted in balsam before 
examination. 

Inasmuch as not infrequently some otlier bacteria besides the tubercle bacilli retain 
a slight red color, it is w^ell, after the specimen is rinsed in water, to float the cover 
glass for a few minutes in a dilute aqueous solution of methylene blue, which will re- 
place the red color in all of the bacteria except the tubercle bacilli and which might be 
mistaken for it, forming a marked color contrast between them. The contrast stain 
should not be intense. 

In Sections. — Thin sections of tuberculous tissue wiiich has been hardened in alco- 
hol are stained in the same way, except that instead of drying and fixation by heat the 
sections should be fixed to the cover glass by means of the albumin fixative (see page 
52), and then cover glass and section are manipulated together. 

When differentiation is complete the section is cleared in oil of origanum and 
mounted in balsam. 



THE INFECTIOUS DISEASES. 225 

For purposes of simple recognition of the bacilli in sections it seems to the writer 
usually better to have no color in the preparation other than that which the tubercle 
bacilli possess. But it is often convenient to demonstrate the nuclei of the cells at the 
same time, and this may be accomplished by staining lightly afterward with a dilute 
solution of some color which will contrast w^ith that of the bacilli, such- as methylene 
blue. 

In the examination of urine for the presence of the tubercle bacillus it is well to 
collect the sediment by means of a centrifugal machine. In the examination of milk, 
or other fat-containing fluids for tubercle bacilli, it is well, after the film has been 
formed upon the cover glass and before staining, to rinse with chloroform followed by 
alcohol, and this by water. 

Occasionally one finds in urine acicular crystalline bodies considerably resembling 
the tubercle bacillus in size and shape, and retaining a red color after the decolorization 
of the specimen. A careful study of the form, however, will suffice to prevent mistakes. 

The only other bacilli which are liable to be mistaken for the tubercle bacilli are 
the bacillus of leprosy and the so-called smegma bacillus which sometimes occurs be- 
neath the prepuce. The lepra bacillus may be distinguished from the tubercle bacillus 
by the following differential staining process: If the lepra bacillus be stained for ten 
minutes in a dilute alcoholic solution of fuchsin (five drops of saturated alcoholic solu- 
tion of fuchsin to 3 c.c. of water), and then rinsed for a few seconds in a solution of 
nitric acid (one part) in alcohol (ten parts), it will retain a red color, while under the 
same treatment the tubercle bacillus remains uncolored. For differential stains for the 
smegma baeillus see page 229. 

Varieties of Tubercle Bacilli. 

While many of the lower mammalia are susceptible to inoculations with tubercle 
bacilli derived from man, the bacilli obtained from spontaneous tuberculous lesions in 
the lower animals may present noteworthy variations in form and growth from the 
human type. Thus Theobald Smith has pointed out marked peculiarities of the bovine 
bacillus which would lead to the conjecture that though not a separate species it is 
probably a distinct variety of the organism. 

Still more marked are the differences between mammalian and avian or bird tuber- 
cle bacilli. Whether in this case also the differences are to be regarded as specific or 
within the limits of variational sway is not yet clear. Although the subject is impor- 
tant from the standpoint of prophylaxis and interesting from the point of view of the 
variations of bacteria under changes of environment, the attempts by experimental 
means to convert one form into the other have thus far been too few to lead to definite 
conclusions. 

Tuberculin. 

When the tubercle bacillus is grown on glycerinated nutrient broth certain meta- 
bolic products are formed and pass into solution in the fluids. If after some weeks of 
vigorous growth the germs are separated by filtration and the broth is concentrated by 
evaporation, a dark-brown fluid results which is called tuhercuUn. This substance^at 
one time believed by man3^ and still by a few observers, to possess distinct curative 
properties in certain forms of tuberculosis — has assumed great economic importance on 
account of its value as a diagnostic agent in bovine tuberculosis. For it is found that 
if administered subcutaneousl}^ in small quantity to cattle, a definite and marked tem- 
perature reaction follows in tuberculous animals, w^hile those which are sound are un- 
affected. The existence of even very slight lesions may be detected in. this way. In 
man also tuberculin has proved of value in cases in which the efforts to establish a 
diagnosis by the usual method have proved futile. 

AcTiox OF Dead Tubercle Bacilli. 

It has been found that tubercle bacilli which have been killed by 
boiling or otherwise, when introduced into the body of the rabbit either 
beneath the skin, or into the serous cavities, or into the blood-vessels and 
15 



226 THE INFECTIOUS DISEASES. 

the air spaces of the lungs, are capable, as they slowly disintegrate, of 
stimulating the cells of the tissues where they lodge to proliferation, 
and to the production of new tissue morphologically similar to tubercle 
tissue in its various phases' (Fig. 119). I^ecrosis of the new-formed 









r^ 




■4 



Fig. 119.— Inflammatory Nodule (Pseudo-Tubercle) in the Liver of the Rabbit Induced by 
THE Intravenous Injection of Dead Tubercle Bacilli. 

Most of the dead bacilli have disintegrated, setting free the bacterial proteid which has stimulated the new 
cell growth. A few fragments of the bacilli, however, still remain. 

cells may occur, but this differs in some respects from the coagulation 
necrosis induced under the usual conditions. Dead tubercle bacilli are 
also markedly chemotactic and capable of causing local suppuration and 
abscess. 

It would seem probable then that while the power of the tubercle 
bacillus to induce necrosis and the fever which in many cases indicates a 
systemic intoxication may be due to metabolic products of the living 
germ, the local lesions characteristic of exudative and i^roductive inflam- 
mation may be due to a peculiar bacterial proteid which is set free by the 
disintegration of the bacilli in the tissues. 

Complex Factors in the Tuberculous Process. 

It is well in studying the characters of tuberculous inflammation to remember that 
in its jorogressive phases there are two factors at work : first, those which lead to cell 
proliferation and new tissue formation, which is apparently a reparative and conserva- 
tive process ; second, those which are inhibitory or damaging or destructive ; and, finally, 
that both sets of factors are commonly active together. It may still be considered doubt- 

^ For further details concerning the effects of dead tubercle bacilli in the body see 
Prudden and Hodenpyl, New York Medical Journal, June 6th and 20th, 1891, and Priid- 
den, ibid., December 5th, 1891. 



THE INFECTIOUS DISEASES. 227 

ful whether the tubercle bacillus furnishes a direct formative stimulus, or whether such 
is furnished by damaged cells, or whether the cell proliferation may not be an expression 
of reparative activity in the presence of damaged tissue made possible by disturbed 
organic control, see page 273. In any event the new tissue which forms under the in- 
fluence of the tubercle bacillus apparently owes its morphological as well as biological 
characteristics to impulses toward tissue formation which are exerted in the presence of 
agencies — doubtless poisons — restraining within narrow bounds the new connective- 
tissue growth, no matter how extensive or persistent this may be, and tending con- 
stantly to its destruction. 

It is interesting in this connection to note that when lesions in many respects simi- 
lar to those of the ordinary tuberculosis are induced experimentally in animals with 
dead tubercle bacilli (see above), the poisonous substances leading to necrosis are not 
produced continually and for indefinite periods, as is the case in infection with living 
bacilli, but are soon exhausted, so that after a certain amount of initial necrosis the new 
tissues go on to develop in the usual reparative way, blood-vessels are formed, and heal- 
ing by a cicatrix under favorable conditions regularly takes place. It is probable that 
effective healing in tuberculosis in man takes place only after the local production of 
destructive poison ceases through the death or diminished virulence of the tubercle 
bacilli present. 

The Number of Tubercle Bacilli in Lesions. 

The number of bacilli which are present in the lesions of tuberculosis 
is subject to great variation. They are usually abundant in the walls 
and contents of phthisical cavities, and in tubercle tissue which is under- 
going cheesy degeneration and disintegration. In these situations they 
may be found in myriads, forming sometimes a large part of the disin- 
tegrated mass. They are found in cells and scattered among them. 
Sometimes they are present in considerable numbers in the giant cells of 
miliary tubercles. In the acute general tuberculosis of children they 
are often present in large numbers, particularly in the lungs (Fig. 115). 
They may be found in tuberculous inflammation in any part of the body, 
and have been seen in the blood. The bacilli are almost constantly dis- 
charged in the sputa of patients suffering from pulmonary tuberculosis, 
often in enormous numbers — from one to four billion in twenty-four hours, 
according to Nuttall's estimate — and their presence sometimes affords 
valuable diagnostic aid in early stages of obscure forms of the disease. 

Under a variety of conditions, especially in the older tuberculous 
lesions, the bacilli may not be demonstrable. This apparent occasional 
absence of the bacilli is probably due either to their disappearance as 
the process grows older, or to some unknown changes which interfere 
with the ordinary staining procedures. 

Frequency of Tuberculosis in Man and the Lower Animals. 

Tuberculosis is a very common disease not only of man' but also of 
many of the lower animals,^ especially of cattle, and inasmuch as the 

^ Carefull}- prepared statistics show that tuberculous lesions are present in the body 
in more than ninety per cent of the cases examined at autopsies. See for a thorough 
and suggestive analysis of five hundred autopsies Naegeli, Virchow's Archiv, Bd. clx., 
p. 426, 1900. 

2 For bibliography of animal tuberculosis see Eher, Lubarsch and Ostertag's " Ergeb- 
nisse," Jahrg. iv. for "1897, p. 859. 



228 THE INFECTIOUS DISEASES. 

victims of this disease, both men and animals, are apt, as stated above, 
to throw off enormons nnmbers of the bacilli in the sputum and other 
excreta, the germ is widely dispersed in inhabited regions, especially in 
buildings frequented by uncleanly tuberculous persons or by infected 
cattle. 

Among the lower animals, guinea-pigs, rabbits, monkeys in confine- 
ment, and cattle are particularly susceptible to the action of the tubercle 
bacillus. Although tuberculosis is widespread in man, he is not, as com- 
pared with some of the lower animals, particularly susceptible. While 
the tuberculous process presents some special differences in different 
animal species in rate of development, amount of necrosis, tendency to 
softening, calcification, etc., the fundamental effects are similar in man 
and in the lower animals. 

Sources of the Tubercle Bacilli, Portals of Entry, and 
Distribution of Lesions. 

There is no doubt that the bacilli may be introduced into the alimen- 
tary canal by the contaminated milk and the meat of tuberculous cattle. 
They may be transmitted from the sick to the well by means of the spu- 
tum, which is allowed to dry and becomes pulverized and which is inhaled 
as dust, and this, under the ordinary conditions of modern life, is the 
chief means of infection. 

Whether the tubercle bacillus can enter the tissues of the body 
through intact mucous membranes, or whether a lesion, however minute, 
is a necessary condition is not yet fully determined. Many observations 
on the occurrence of tuberculous bronchial lymph-nodes in persons ex- 
hibiting no appreciable tuberculous lesions elsewhere would indicate the 
IDrobability of access of the bacilli to the lymph channels without pri- 
mary lesion at the portal of entry. A considerable percentage of persons- 
dying from other diseases have been found to have tuberculous lesions 
often healed in the lungs or bronchial lymph nodes.' In adults the 
lungs, in children the bronchial lymph- nodes are the most frequent seat 
of tuberculous lesion. ' 

Concurrent Infection in Tuberculosis. 

A concurrent infection with the tubercle bacillus and the pyogenic 
micro-organisms is of extreme significance in that phase of tuberculous 
inflammation of the lungs commonly called i^hthisis." While the so- 
called cold abscesses may be caused by the tubercle bacillus alone, this 
germ is not infrequently found under these conditions to be associated 
with other pyogenic micro-organisms, especially the streptococcus and 
staphylococcus. 

^ See reference Naegeli, p. 227. 

'^ See reference, Northru/p and Bovaird, p. 443. For a study of tlie distribution and 
origin of tuberculosis in children see Guthrie, Lancet, February 4tli, 1899, p. 286. 

^ See Spengler, Zeitschr. f. Hj^giene, etc., Bd. xviii., p. 342, 1894, bibliography. See 
reference to Pruddeii, p. 478. 



THE INFECTIOUS DISEASES. 229 



Bacteria Resembling the Tubercle Bacillus. 

The SMEG:\rA Bacillus. — This organism is often present and sometimes in large 
numbers in the preputial smegma and elsewhere about the external genitals. It so 
closely resembles the tubercle bacillus in size, shape, and staining reactions that it is 
liable by morphological examinations alone to be mistaken for it. It has been cultivated 
on artificial media and is not pathogenic. The smegma bacillus, although when treated 
by the method above recommended for staining the tubercle bacillus resists the decolor- 
izing action of the acid, is nevertheless usually decolorized by alcohol ; in this respect 
differing from either the tubercle bacillus or the leprosy bacillus. But this color reac- 
tion is not certain ; individual bacilli not infrequently remain unstained. Various spe- 
cial methods for differentiation have been suggested, but none of them is wholly 
satisfactory.! In doubtful cases, therefore, and especially wdien serious operative pro- 
cedures are dependent upon the bacterial diagnosis, recourse should be had to animal 
inoculations. 

The " Hay Bacillus. " — This is another bacillus resembing the tubercle and smegma 
bacilli in form and staining peculiarities, recently described b}^ Moeller. It is called 
the " hay bacillus " or " grass bacillus " because of its common occurrence upon grass 
heads in the fields. This organism is not pathogenic, is readily cultivated, and is chiefly 
of interest because it completes another illustration of bacterial groups of apparently 
related organisms, some of which are harmless saprophytes, others strictly and signifi- 
cantl}^ parasitic. 

Lupus and Other Forms of Tuberculosis of the Skin. 

Local tuberculous inflammation of the skin may occur in the form of small nodules 
or wart-like thickenings, as the result of accidental inoculation. Local skin infection 
may occur about the orifices of the body in tuberculous persons from contact Avith secre- 
tions or excretions containiog the tubercle bacilli, or about sinuses leading to tubercu- 
lous abscesses, joints, etc., or in the vicinity of tuberculous lymph-nodes. 

A chronic form of tuberculous inflammation which presents special clinical features 
has long been known under the name of lujnis. ' 

Lupus. — This form of inflammation most frequently occurs in the skin of the face, 
but also in the mucous membrane of the mouth, pharynx, conjunctiva, vulva, and 
vagina. The lesion consists of small, multiple nodules of new-formed tissue, in the cutis 
or mucosa and submucosa. By the formation of ncAv nodules and a more diffuse cellu- 
lar infiltration of the tissue between them, the lesion tends to spread, and by the conflu- 
ence of the infiltrated portions a dense and more or less extensive area of nodular in- 
filtration may be formed. There may be an excessive production and exfoliation of 
epidermis over the infiltrated area, or an ulceration of the new tissue. 

Microscopical examination shows the lesion to consist of small spheroidal cells in- 
termingled with variable numbers of larger, polj^hedral cells and cell masses, and in 
many cases giant cells (Fig. 120). In some cases a well-marked reticulum is present 
between the new cells, and these are often grouped in masses around the blood-vessels. 
In some cases there is, without previous ulceration, a formation of new connective tis- 
sue in the diseased area, and a well-marked cicatrization ; in other cases the cells and 
intercellular substance undergo a disintegration which leads to ulceration. Tubercle 
bacilli in small numbers may be found in these lesions. In the clinical group of diseases 
called lupus there are other forms of lesion which are not incited by the tubercle 
bacillus. 

Bibliography of Tuberculosis. 

The announcement of the discovery of the bacillus tuberculosis by Koch was made 
in the Berliner klin. Wochensclirift, 1882, No. 15. A most elaborate and valuable article 

^ Critical review, with bibliographv, DcOims, Journal American Medical Association, 
vol. xxxiv., pp. 983 and 1045, 1900. 

Consult also Coicie, Jour. Exp. Med., vol. v., p. 205, 1900. 



230 



THE IISTECTIOUS DISEASES. 



on the same subject by Koch is contained in the " Mittheilungen aus dem Kaiserlichen 
Gesundheitsamte," vol. ii. 

The abundant literature on the subject of the tubercle bacillus which has accumu- 
lated since 1883 is for the most part scattered through the Gennan, English, and French 
journals. 

An excellent critical resume of the subject \)j Lartigau, with selected bibliography, 
may be found in the "Twentieth Century Practice," vol. xx. 








rSf<!>^ ** * ' 




*>^ 



■.^^^ 



^ -^^-r^ ^:«'-^>-^i£™i. 



--^^>-^%^l^- 



Fig. 120.— Lupus of Face. 



In the large work of Straus, " La Tuberculose, " 1895, the experimental aspects of 
the subject are fully considered. 

In the w^ork of Cornet, "Die Tuberculose," 1899, together with the general and 
clinical consideration of the disease, the modes of infection and prophylaxis are set 
forth, with bibliography. 

LEPRA (LEPROSY). 

Leprosy is characterized by the development of nodular and some- 
times diffuse masses of tissue, consisting of larger and smaller cells of 
various shapes — spheroidal, fusiform, and branched, mth a fibrous 
stroma — the whole somewhat resembling granulation tissue. The new 
tissue is most frequently formed in exposed parts of the skin, as the 
face, hands, and feet, but it may occur in the skin of any part of 
the body. It is formed more rarely in the subcutaneous connective tis- 
sue, in intrafascicular connective tissue of nerves, in the viscera, and in 
the mucous membranes. The mucous membranes most frequently af- 
fected are those of the eye, nose, mouth, and larynx. The nodules may 



THE INFECTIOUS DISEASES. 231 

be very small or as large as a walnut, and may be single or joined to- 
gether in groups or masses. The tissue of the part in which the new 
formation occurs may be atrophied and replaced by, or may remain in- 
termingled with, the leprous tissue, or it may be hyperplastic. The 
nodules may persist for a long time without undergoing any apparent 
change, or they may soften and break down, forming ulcers ; but ulcer- 
ation, except in the mucous membranes, is said usually to occur as the 
result of injury or unusual exposure. The leprous tissue may change 
without ulceration into cicatricial tissue, or cicatrization may follow 
ulceration. 

Various secondary lesions and disturbances of nerve function are 
associated with the formation of leprous tissue in the nerves and central 
nervous system, but these we cannot consider here. 

In all the primary lesions of leprosy, bacilli are said to be present, 
mostly in the cells, and particularly in the larger transparent si^heroidal 
forms, but sometimes free in the intercellular substance. The bacilli 
have been found in the skin, mucous membrane of the mouth and 
larynx, in peripheral nerves, in the cornea, in cartilage, in the testicles, 
and in lymph-nodes. Sometimes the cells contain but few bacilli, but 
they are frequently crowded with them. 

Characters of the Lepra Bacilli. 

The bacilli are from 4 to 6 /^ long and very slender. They are sometimes pointed 
at the ends and sometimes present spheroidal swellings (Fig. 121). In their comport- 
ment toward staining agents, as well as in general morphological characters, they 
considerablj^ resemble the Bacillus tuber- 
culosis, but they are more readily stained. 
They may be stained with fuchsin or 
gentian violet bj^ the ordinary method, 
or by the method employed for staining 
the tubercle bacillus (see page 223). 

Various reports of success in the arti- 
ficial cultivation of the lepra bacillus have 
not yet received the seal of experimental 
confirmation. 

The lepra bacillus may be conveyed 
from man to man by direct inoculation; 
but under proper sanitary conditions the 
disease is rarely initiated in this way. In 
a few cases animal inoculations have been fig. 131.— The Bacilli of Leprosy. 

made with what appear to be positive From a nodule in the skin, showing the bacilli free 
results. ^ and within cells. 

The structure of the new tissue growth, the absence of coagulation 
necrosis, and the peculiar grouping of the bacilli in the large transparent 
cells are characters which usually clearly distinguish the lesions caused 
by the leprosy bacillus from those of tuberculosis. 

Leprosy is common in India and in other hot countries. It is infre- 
quent in America, but in the Gulf States, in Mexico, among the l^orwe- 

^ For full bibliography of leprosy consult Morroic, " Twentieth Century Practice, " 
vol. xviii^ 




232 



THE INFECTIOUS DISEASES. 



gians in the I^orthwest, and in the eastern British provinces a considerable 
number of cases are grouped. Isolated cases are, however, encountered 
now and then in various parts of the United States. 




Fig. 123. 



SYPHILIS. 

The characteristic lesions of syphilis consist in a more or less circum- 
scribed formation of new tissue. This may be made up largely of small 
spheroidal cells or of these with polyhedral cells (Fig. 122), and of occa- 
sional giant cells. The new tissue, which may be diffuse or in more or 
less clearly circumscribed masses, contains, as a rule, few blood-vessels, 

and is prone to undergo coagu- 
lation necrosis. This tendency 
is most x)ronounced in the cir^ 
cumscribed masses. 

The endothelial cells of the 
blood-vessels in and near the 
inflammatory foci in this form 
of inflammation are not infre- 
quently swollen and may pro- 
liferate (Figs. 122 and 123, B). 
The vessels may otherwise un- 
dergo extensive changes. 

In the primary lesion, which 
is called chancre, there may be 
obliterating endarteritis, a 
small spheroidal -cell infiltra- 
tion of the connective tissue, 
proliferation of connective-tissue cells, especially near the blood-vessels 
(Fig. 124), swelling of the vascular endothelium, and an occasional de- 
velopment of giant cells. This new tissue may become fibrous or ne- 
crotic and may ulcerate. 

Following the primary lesion there may be inflammation of the lymph 
nodes, of the skin and mucous membranes, of the bones and viscera. 

One of the most characteristic phases of the secondary inflammations 
of syphilis results in the formation in the j)eriosteum or the viscera of 
masses of new tissue called gummata. 

The smaller gummata consist of a mass of small spheroidal and epi- 
thelioid cells (see Fig. 125). As these cell masses grow larger they are 
apt to become necrotic and caseous at the centre, and we may then have, 
as seen by the naked eye, a grayish-white, usually firm mass, with a more 
or less dense and irregular granular centre and a translucent, often 
radially striated border of dense fibrous tissue (see Fig. 126). 

A bacillus closely resembling the tubercle bacillus in form and size 
has been described by Lustgarten and others as occurring in small num- 
bers in the lesions of syphilis. It appears not to be constantly present, 
however ; a distinctly characteristic mode of staining is not known, and 



From 



-New-formed Tissue in Syphilitic Inflam- 
mation. 

hard chancre," showing swollen endothelium in 
a small blood-vessel. 



THE INFECTIOUS DISEASES. 233 

it has never been cultivated on artificial media ; so that the evidence that 
this bacillus is the excitant of syphilitic inflammation is not convincing. 
Several other organisms have been described as occurring in syphilitic 
lesions, but in no case has satisfactory evidence of their significance as 
excitants of the disease been furnished. 

The nodular lesions of syphilis are in many respects structurally 
similar to those of tuberculosis, so that it is sometimes difficult to distin- 



\j\.\^r 






c -^ 






• -1 *^'' "ff, I^fci, *"" J * , ji K * c ^>«,A<i \ L 



B-v- -r'K-^' ->V. ^ ' ;•- . sA«'' 

^'■^^ //^ -vl? -">.\u^^*~^V-,^. 

































Fm. 133.— Section of A Portions of a Syphilitic Condyloma of the Mucous Membrane. 

A, (Edematous papilla ; B, swollen endothelial cells in small blood-vessels of a papilla ; C, pus cells in 
ttie submucous connective tissue ; D, pus cells in the epithelium ; E, disintegration of the epithelium in the 
superiicial portion of the mucous membrane. 

guish them on mophological examination alone. But the greater variety 
in the developmental stages of the tuberculous foci which may be found in 
a single individual ; the grouping of the lesions in a manner indicative of 
local infections, and in the last resort the demonstrtation of the presence 
of the tubercle bacillus, will usually suffice to distinguish the tuberculous 
from the syphilitic lesion, even without recourse to the clinical history. ' 
For further details regarding syphilitic lesions of the viscera see Part 
III. 

^ For critical summary of syphilis with recent bibliography see Lang and UUmann 
in Lubarsch and Ostertag's " Ergebnisse, " Jahrg. v. for 1898, p. 481. 

For a study of blood-vessel changes in syphilis with bibliography see Abramow, 
Ziegler's Beitrage, Bd. xxvi. , p. 202. 



234 



THE INFECTIOUS DISEASES. 

















Fig. 124.— S' ction prom a primary Syphilitic Nodule of the Mucous Membrane op the Mouth. 
Showing collections of cells about the blood-vessels in the submucous tissue. 



_^ ^'^V^->^ 




Fig. 135.— Small Nodulf of Syphiiitic Inflam- 
mation (Miliary Gumma) in the Liver. 



Fig. 136.— Syphilitic Gumma in the Liver. 
Showing necrotic caseous centre merging into 
the new-formed cellular and fibrous tissue in the 
periphery. This gumma was much larger and is 
much less magnified in the cut than Fig. 135. 



THE INFECTIOUS DISEASES. 235 



Rhinoscleroma. 



This disease, which occurs especially in eastern Europe and occasionally in other 
parts of the world, is a chronic inflammation of the nasal, pharyngeal, and laryngeal 
mucous membrane. In this inflammation a difi'use or nodular formation of new tissue, 
somewhat resembling granulation tissue, occurs, which tends to assume a dense cicatri- 
cial character. 

Constantly associated, it is said, with this lesion is a bacillus called Bacillus rhino- 
scleromatis. This bacillus in most of its morphological and biological characters closely 
resembles the pneumobacillus of Friedlander, growing readily on the common culture 
media and developing a capsule, and it may be identical with it. 

The relationship of this bacillus to the lesions of rhinoscleroma does not appear to 
be as yet definitely established, since inoculations in men and animals have not given 
positive results. 

DIPHTHERIA. 

Diphtheria is an acute infectious disease incited by the Bacillus diph- 
therice (Loffler), and usually characterized by a pseudo-membranous in- 
flammation on some of the mucous membranes or occasionally on the 
surface of wounds, and by immediate or remote effects of absorbed toxic 
substances. The mucous membranes which are the most frequently 
affected in diphtheria are those of the tonsils, pharynx, soft palate, 
nares, larynx and trachea; less frequently those of the mouth, gums, 
conjunctiva, oesophagus, and stomach. 

Morphology of the Lesions. 

The local lesions in mucous membranes may present various phases, 
which represent clinical types of the disease. Thus there may i)e a sim- 
ple redness of the affected surfaces which leaves no trace after ceath, or 
there may be a simple catarrhal inflamma- 



>^„ 



tion. On the other hand, in the more kfc' 
marked forms of the lesion there may be a 
fibrinous exudate which infiltrates the mu- 
cous membrane, or, intermingled with pus 
cells, epithelial cells, red blood cells, bacteria, 4 
and granular material, forms a thick or thin .. . 
pellicle on the affected surfaces (see Fig. 94, ^ '>^>*'^ 

p. 186). This pellicle may undergo coagula- 
tion necrosis (Fig. 127), and hand-in-hand J* T^ -^ ^ 'j; 
with this there may be superficial or deep '" *^ ' ~" ~ 
necrosis of the mucous membrane. The fig. 12T.-fibrin m diphthkritic 

„, - -Tiji ■ ' ji n 1 Membrane undergoing Coagula- 

lalse membrane m diphtheria is thusiormed ^jq^ necrosis. 
by a combination of inflammatory products 

and necrotic tissue, the extent of the necrosis and the amount of inflam- 
matory products varying in different cases. The membrane may disin- 
tegrate or exfoliate, with or without loss of tissue in the underlying mu- 
cous membrane. Phlegmon, abscess, and cedema are liable to occur as 
local complications. 



236 THE INFECTIOUS DISEASES. 

Adjacent and distant lymph- nodes are apt to be swollen, and often 
show, on microscopical examination, endothelial -cell hyperplasia with 
small foci of cell necrosis and disintegration.' Similar foci of cell 
hyperplasia with necrosis with small spheroidal- cell accumulation and 
fatty degeneration may be found in the kidney, spleen, and liver. Al- 
buminous degeneration in the kidney and acute nephritis are not infre- 
quent. Small hsemorrhagic foci may be present in the liver and kidneys. 
Degeneration of the heart muscle may occur. ^ The exact nature of the 
nerve lesions which may be associated with the late paralyses of diph- 
theria is not yet clear, but degeneration of the peripheral nerves and 
chromatolysis of the ganglion cells occur, indicating the action of an 
absorbed toxic substance in the body fluids. Leucocytosis may be pres- 
ent. 

Catarrhal bronchitis and broncho -pneumonia or simple lobular pneu- 
monia frequently complicate diphtheritic lesions of the upper air pas- 
sages and fauces. 

Bacteriology of the Disease. 

Although bacteria of various forms are commonly present in the false 
membrane, and some of them ]3enetrate deeply into the underlying tis- 






Fig. 128.— DiPHTHEKiTic Inflammation of the tonsil. 
Showing Loffler's bacilli in the pseudo-membrane. 

sue, the primary and specific excitant of this disease is the Bacillus diph- 
therise of Loffler. 

In man the diphtheria bacilli are largely confined to the seat of local 
lesion, and sometimes occur here in enormous numbers, especially in the 

1 Consult Waschkewitsch, Virch. Archiv, Bd. clix., p. 137, 1900. 

1 For studies of the lesions of the myocardium in diphtheria consult Scagliosi, Vir- 
chow's Arch., Bd. cxlvi., p. 115, 1896; also Thomas and Hihhard, Reports of Boston 
City Hospital, 1900, p. 204, bibl. ; for a study of nerve lesions with bibl. see Batten, 
Pediatrics, vol. vii., p. 97, 1899; also Rainy, .Jour. Path, and Bact., vol. vi., p. 435, 
1900. For a comprehensive study of the bacteriology and pathology of two hundred 
and twenty fatal cases of diphtheria see Councilman, Mallory, and Pearce, Jour. Boston 
Soc. Med. Science, vol. v., p. 139, 1900. 



THE INFECTIOUS DISEASES. 237 

older layers of the pseuclo-membraue (see Fig. 128). But they may 
become widely distributed through the body. This appears to be espe- 
cially the case when the pyogenic cocci are associated with the diphtheria 
bacillus at the seat of local lesion. The systemic effects in diphtheria 
appear to be largely due to the absorption into the body of toxic material 
elaborated locally by the germs. Septicaemia or acute visceral inflam- 
mations, particularly of the kidney, may occur without evidence of an 
external local lesion or of the portal of entry of the bacillus. ' 

Concurrent Infections. 

The very frequent association of the pyogenic cocci and other bacteria 
with the diphtheria bacillus gives rise to a series of changes which make 
the clinical picture and the lesions of diphtheria sometimes very com- 
plex. Thus the complicating bronchitis and broncho -pneumonia, as well 
as pysemic symptoms and lesions, may be due to the diphtheria bacillus 
alone. But these secondary lesions may be due to the presence in the 
pseudo -membrane, and the entrance into the deeper air passages and the 
blood, of Streptococcus pyogenes. Staphylococcus pyogenes, Diplococcus 
lanceolatus, Bacillus coli communis, and other bacteria, or of these to- 
gether with the diphtheria bacillus.^ 

Characters of the Diphtheria Bacillus. 

This organism, first described and definitely associated with this disease by Loflfler, 
is a slender rod, in general about 3 // long, but sometimes shorter and sometimes growing 
into threads. It occasionally grows in branching forms, ^ and is characterized morpho- 
logically by marked irregularities in its form (Fig. 129). 
While the typical form is that of a round -ended, straight, ^[ M 

or slightly curved bacillus, it is very apt — perhaps as a % /W\ i^ 

result of degeneration — to appear club-shaped or pointed 
at the ends, irregularly segmented, and to develop at the 
ends or elsewhere a strongly refractile material which 
stains more deeply than the rest of the protoplasm. 

The diphtheria bacillus is immobile, asporogenous, 

grows best at blood heat, and thrives on most of the arti- t, -.«» ^ ^ 

2 . T fl -1 -^ 1 1 -11 ^ 1 ^^^- 129. — Bacillus Diphthe- 

ficial culture media. In fluids it may be killed by an ex- j^j^g 

posure of ten minutes to a temperature of 58° C. ; but it 

, . p , ^1 • p j_ From exudate in the throat of a 

may remain alive for weeks, or even months, m fragments ^^^^ ^^ diphtheria : showing ir- 

of dried membrane. It may be stained with Lofller's al- regularities of the bacilli in shape 
kaline methylene -blue solution or by Gram's method. and size and coloration. 

The diphtheria bacillus is subject to extreme varia- 
tions in virulence, forms occurring which with all the usual cultural characteristics are 
not in the slightest degree virulent. 

^ For a resume and bibliography of studies relating to diphtheritic septicsemia see 
Browa and Thiry, Gazette des Hopitaux, May 2d, 4th, and 9th, 1899. 

'' For a study of the presence and action of the diphtheria bacilli in the lungs see 
Flexner and Anderson, Johns Hopkins Hospital Bulletin, vol. ix., p. 72, 1898. 

For a summary of the association of diphtheria and tuberculosis see Councilman, 
Mallory, and Pearce, reference above. 

^ The branching forms which are occasionally observed in the diphtheria as well as 
in the tubercle bacillus, together with certain other characters, have led some observers 
to the belief that these organisms are related to streptothrix and to the moulds rather 
than to the bacteria. But, for the present at least, it seems wiser to consider it in its 
more generally acknowledged relationships. 




238 THE INFECTIOUS DISEASES. 



Action of the Bacillus in Animals. 

Inoculations of virulent cultures subcutaneously in guinea-pigs are followed by a 
localized hemorrhagic oedema with a variable amount of whitish exudate. Death usu- 
ally occurs in from two to five days. In addition to the local lesions there may be— but 
this is not constant — swelling of the adjacent and of the abdominal lymph-nodes, serous 
effusions into the pericardial, pleural, and peritoneal sacs ; swollen spleen, albuminous 
and fatty degeneration in the liver, kidney, and heart muscles ; congestion and some- 
times hemorrhage of the suprarenals. Microscopical examination shows, in a consider- 
able proportion of cases, fragmentation of nuclei and other evidences of cell death at 
the seat of inoculation and in the viscera, as well as chromatolysis of ganglion cells in 
the anterior horn. Animals which survive the inoculations may later develop paraly- 
sis, and a similar result may follow the injection into rabbits of culture fluids. The 
bacilli do not usually gain access to the body at large, but may be found at the seat of 
inoculations. Inoculation into the mucous membranes of rabbits, pigeons, and certain 
other animals may result in the development of a pseudo-membrane somewhat resem- 
bling that of the disease in man. 



Diphtheria Toxin and Antitoxin. 

During the growth of the diphtheria bacillus in nutrient broth an 
allwiminous toxic substance is developed which mingles with the broth. 
This is called diphtheria toxin, and subcutaneous injections of this toxin 
in animals — guinea-pigs, for example — proves fatal, in appropriate dos- 
age, with symptoms and lesions similar to those caused by inoculation 
with the living germ. It has been found that by repeated injections of 
the diphtheria toxins in susceptible animals, at first with small, then with 
gradually increasing doses, the animal may at length become so insuscep- 
tible to the action of the poison that many times the usually fatal dose is 
borne without sensible reaction. Similar immunity can be conferred in 
certain animals by the use of the living cultures of the diphtheria bacil- 
lus either fully virulent or with reduced virulence (see p. 170), adminis- 
tered at first in small doses which are gradually increased. 

In whichever way immunity be conferred, it has been found that the 
blood of the artificially immunized animal contains a substance, or sub- 
stances, called diphtheria antitoxin, which, on being introduced with the 
blood serum into other susceptible animals, may not only confer a 
qu] :ly established immunity, but, without destroying the diphtheria 
gen , may protect against its toxic effects when the disease is already 
undur way. Thus through the artificial immunization of horses and 
the hypodermatic use of the serum of their blood in man the so-called 
^^ serum therapy" has assumed a very important and beneficent role in 
the prevention and treatment of diphtheria. ' 

^ For further details regarding methods of bacterial diagnosis in diphtheria, and of 
the manufacture and tests of the antitoxin, consult Park, "Bacteriology in Medicine and 
Surgery," 1899. It is important from the prophylactic standpoint to remember that 
the Bacillus diphtherias may remain alive in the mouth of the human subject for many 
weeks after recovery from the local lesions of the disease, and also that healthy persons 
when the disease is prevalent may harbor the virulent bacilli in their mouths. 



THE INFECTIOUS DISEASES. 239 



Other Bacteria of the Diphtheria Bacillus Group. 

While the diphtheria bacillus varies greatly in the physiological capacities which 
deterniine its virulence, its general morphological and cultural characteristics are lairly 
constant. There are, however, non-virulent bacilli occurring on mucous membranes 
under normal as well as abnormal conditions which considerably resemble this, but 
which differ somewhat in both morphological and biological characters from the true 
diphtheria bacillus and its variants. Such organisms have been called pseudo-diplitheria 
'bacilli. These non-virulent form" may be regarded as attenuated varieties of the diph- 
theria bacillus. 

The so-called Xerosis bacillus, which has been repeatedly found in xerosis conjunc- 
tivge, is apparently a member of the diphtheria bacillus group. 



TETANUS. (Lockjaw.) 

This disease, which is especially marked clinically by muscular spasm, 
is due to infection by the Bacillus tetani. This organism is rather wide- 
spread and in some places very abundant, occurring with other germs in 
the soil, esjDecially in manured soil, and gaining entrance to the body 
through wounds, which are often very slight. The soil in certain regions 
appears to harbor in especial abundance the tetanus organism or its 
spores. Thus in certain districts on Long Island and in Xew Jersey 
slight injuries are frequently followed by tetanus. The liability to in- 
fection from the spores is greatly enhanced by their association with 
other organisms or with dirt, splinters, etc., in the wound. 

The Lesions of the Disease. . 

The local lesion in tetanus is usually slight and not characteristic, 
often consisting only in a slight supiDuration. 

The morphology of the lesions of the nervous system to the existence 
of which the symjDtoms of tetanus so directly point is yet obscure. Over- 
filling of the blood-vessels, cellular exudate into the perivascular spaces, 
chromatolysis of the ganglion cells of the spinal cord are common. The 
bacillus remains for the most part at the seat of local lesion and induces 
its effects by the elaboration of a most intense poison or toxin, called 
tetano-toxin. The action of this toxic substance appears sometimes to 
continue in the body after the death of the organisms which have e jor- 
ated it. This infectious disease affords a most typical examjj 3 of 
toxaemia. 

Characters of the Bacillus Tetani. 

It is rather long, slender, and motile, often growing in pairs or threads and prone 
to develop a spore in one end (Fig. 130), in Avhich condition the bacillus is larger at this 
end, being club- or racKet-shaped. It is readily stained. At the room temperature it 
grows on artificial culture media, and is strictl}^ anaerobic, flourishing in an atmosphere 
of hydrogen. It fluidifies gelatin after sending out into it irregular-shaped, ray-like 
outgrowths. 

The spores of the tetanus bacillus are very resistant to drying, to heat, and to vari- 
ous chemical disinfectants. 



240 THE INFECTIOUS DISEASES. 

Characteristic tetanic symptoms followed by death may be induced in mice, guinea- 
pigs, and rabbits by subcutaneous inoculation of cultures. Man and the horse are 
markedly susceptible to tetanus; birds are as a rule insusceptible. If the tetanus ba- 
cillus be grown in nutrient broth at blood heat out of contact with oxygen the toxin is 
developed and mingles with the fluid. This toxin when freed from living germs is 
capable of inducing the symptoms of the disease. Broth cultures may after some 
weeks have acquired such an extreme intensity that the dried poisonous material, sep- 
arated from the inert fluids and partially purified, may be fatal to a mouse weighing 15 
gm. in a dose of 0.00000005 gm. Estimating according to the relative weights of the 
subjects, the minimal fatal human dose would be about 0.00023 gm. This toxin is ren- 
dered inert by a temperature above 65° C. and by light. 

Tetanus Antitoxin. 

By procedures similar to those described in diphtheria immunization 

(p. 238), the tetanus toxin has been used to secure artificial immunity in 

dogs, goats, and horses, and here also the blood serum of the immunized 

animals has been jjrepared and employed in man 

mmm»i^ for thcrapeutic purposes with some degree of suc- 

^ \ <s \^ cess. The theoretical promise of the tetanus an- 

S\^/^ /k titoxin for therapeutic purposes in man is, how- 

mmm^a\ P^A I ever, in practice rendered in large measure futile, 

\^\aw because the existence of the disease is not recog- 

FiG. 130.-BACILLUS TETANi. nizablc uutil thc toxa^mia is sufficiently marked to 

, ^ produce the nervous symptoms, at which time an 

From a culture ; showing club- ^ j x ? 

shaped ends with spores. euomious and not easily determined dosage is re- 
quired to neutralize or counteract the effects of 
the already elaborated poison. Statistics are as yet too meagre to jus- 
tify a final opinion as to the practical value of serum therapy in 
tetanus, but it appears to be definitely useful. ' 

Diagnosis. 

For purposes of diagnosis it may be necessary to inoculate a white 
mouse at the base of the tail with suspicious material at the same 
time that morphological examination and anaerobic cultures are made. 
Should tetanus develop in the mouse within a few days control cultures 
may be made from the exudate at the seat of inoculation. 

Other Bacilli of the Tetanus Group. 

Several bacterial species are already known which may be classed in the tetanus 
group. While varying in size, these bacilli are in general rather large; spores form m 
their thickened ends ; they are facultative anaerobes ; some do, others do not fluidify 
gelatin, and they retain the stain bj' Gram's method. They are mostly saprophytes 
and have been found in milk and milk products, in excrement and sewage, etc. Kone 
are known to be pathogenic in man. The most notcAvorthy among these is Bacillus 
j)seudo-tetanicus, Sanfelice, which in morphology and growth characters resembles the 
Bacillus tetani, but it does not form the toxin. 

^ For a critical resume of tetanus and its treatment with the antitoxic serum, with 
bibliography, see Mosclicoicitz, Annals of Surgery, vol. xxxii., p. 219, 1900. 



THE INFECTIOUS DISEASES. 241 



RELAPSING FEVER. (Typhus Recurrens ; Famine Fever ; Spirillum 
Fever; Seven Day Fever.) 

The lesions which may be present in this disease are not distinctive. 
It is characterized, apart from symptoms, by the presence in the blood 
at certain periods of a spiral bacterium discovered by Obermeier in 1873. 



The Lesioxs of the Disease. 

There may be albuminous degeneration in the \lscera, leucocytosis, 
catarrhal or croupous inflammation of the mucous membranes of the res- 
piratory and digesti\ e organs, ecchymoses in the skin and in the mucous 
and serous membranes. There may be pneumonia and j^leurisy, degen- 
eration of the cardiac muscle, hyperplasia of the mesenteric lymph-nodes. 

The Spleen may be large and flabby, this change being so extreme that 
rupture has occurred duriog life ; it may also be the seat of infarctions, 
and these ha^'e given rise to jDeritonitis. 



Characters of the Spirochsete Obermeieri. 

In the blood of all parts of the body during the febrile attacks may be found, in 
very large numbers, a long, slender spirillum called from its discoverer SpirocJmte Ober 
ineieri (Fig. 131). The organisms disappear from the blood 
during the afebrile intervals, and it has been shown that 
at this time they accumulate in the spleen, where they are 
destroyed in large numbers, apparently through the action 
of phagocytic cells. The organism is from 14 to 40 ix in 
length, and performs rapid, undulating movements. 

The inoculation of healthy men and of mon- 
keys with the blood of relapsing-fever patients 
which contains the bacteria, induces a similar ^^^- '^^-"l^il^'f^"" ''^^^- 

-Mli.lr.Kl. 

disease. Pure cultures have not as yet been 

made of these bacteria, but for the reasons indicated, and since the or- 
ganism has never been found except in connection with the disease, there 
is every reason for believing that the Spirochsete Obermeieri is the exci- 
tant of relapsing fever. 

Malta Fever. 

This disease, which has been most frequently observed along the shores of the 
Mediterranean and in India, is characterized by prolonged pyrexia with irregular re- 
missions. In the rather rare fatal cases there may be considerable enlargement of the 
spleen, albuminous degeneration in the liver and kidneys. Acute nephritis may occur. 

It is said that there are constantly present in the spleen in this disease small cocci 
stained by Gram, readily cultivated on artificial media. The result of inoculations of 
pure culture into monkeys and other animals tends to confirm the pathogenic signifi- 
cance of the organism, which has been called Microcorcu^ i/iehtexsis.^ 

^ Consult Birt and Lamb, Lancet, 1899, ii., p. TOl Bibl. 
16 




242 THE INFECTIOUS DISEASES. 



BUBONIC PLAGUE. (Oriental Plague ; Black Death.) 

Types of the Disease. — This disease presents three main types — the bu- 
bonic, pulmonary, and septicsemic. 

The most common is the bubonic, which is characterized by an intense 
inflammatory hyperplasia of the lymph-nodes, most frequently the in- 
guinal or axillary. The surrounding tissue may be involved ; haemor- 
rhage, necrosis, or suppuration in the nodes may occur. Coincident with 
these local reactions there may be albuminous degeneration, focal necro- 
sis, and leucocytosis from toxaemia, or secondary foci of inflammation in 
the spleen or lungs or liver. A second type of the infection is the pul- 
monayii, in which larger or smaller areas of the lungs are involved in 
broncho-pneumonia with associated secondary involv^ement of the bron- 
chial lymph-nodes. In the septiccemic type of bubonic plague there may 
be a general involvement of the lymph-nodes and nodules of the body 
with the marks of toxaemia, without an indication of the point of primary 
infection. 

In all these various phases of the disease the plague bacillus may be 
present often in enormous numbers in the primary buboes and in the 
secondary lesions and in the viscera ; in the consolidated areas and in the 
sputum in the pulmonary type, and in the septicsemic phases, in the blood. 

Characters of the Plague Bacillus. 

The plague bacillus was discovered in 1894 b}^ Kitasato and Yersin, and its role as 
the excitant of the disease was soon established. It is a short, thick, motile, round-ended 
bacillus, often staining more deeply at the ends than in the middle. It sometimes 
grows in chains and may be capsulated, not forming spores; it is decolorized by Gram's 
method. It grows readily though not voluminously on the ordinary culture media at 
blood heat. This organism is killed by drying for a few days and by exposure to sun- 
light for a few hours. Subcutaneous inoculation in guinea-pigs and rabbits is followed 
by local hemorrhagic and serous inflammation with typical involvement of the regional 
lymph-nodes and b}^ septicaemia. Death may supervene in from one to five or six days, 
and albuminous degeneration of the viscera, hyperplasia of the spleen, and petechial 
hemorrhages may be present. 

Portals of Entry. — The chief portals of entry in man are abrasions or 
wounds of the skin, the lungs, and the intestines. The spread of the 
infectious material in overcrowded and unsanitary districts may readliy 
take i)lace by rats, which are very susceptible to the disease and may be 
infected by feeding. Through mosquitoes and flies also the bacilli may 
be conveyed from man to man or from dead rats or their dejecta to man. 

Preventive Inoculation has been largely practised in the East by the 
Haffkine method. This consists in the subcutaneous injection of beef- 
tea cultures of the plague bacillus, which have been killed by heating. 
Moderate local inflammatory reaction and slight fever may follow the 
injection. The statistics seem to indicate that among exposed persons 
the mortality may be reduced eighty per cent or more by this preventive 
inoculation. 



THE INFECTIOUS DISEASES. 243 

An anti -plague serum, prepared by the immunization of horses, has 
been used by Yersin with at least promising results. ' 



HEMORRHAGIC SEPTICiEMIA. 

There are several bacilli which may be classed, as is done by Hueppe, Kruse, and others, 
with the plague bacillus under the designation, the Immorrliagic septicmmia group. These 
are mostly small, short, sporeless forms growing readily on the ordinary media as facul- 
tative anaerobes, not fluidifying gelatin and decolorizing by Gram. Some of these are 
motile, others not. Among these may be mentioned the bacillus of mouse typhus (B. 
typhi murium), the bacillus of hog cholera (B. suipestifer), the bacillus of chicken 
cholera (B. cholerie gallinarum), the bacillus of swine plague (B. suisepticus). Several 
species related to these and to the plague bacillus are pathogenic in man ; thus the 
B. Tuemorrhagicus septicus of Babes, the B. Immorrhagicus of Kolb, the B. Immorrhagicus 
velenosKS of Tizzoni and Giovanni. 

The recognition of these and related species may be of especial significance in con- 
nection with the diagnosis of bubonic plague by cultures and animal inoculations. ^ 

Bacillus Aerogenes Capsulatus (Bacillus Welchii, Gas 

Bacillus). 

This bacillus was described in 1891-92 by Welch and ^uttall. Later 
studies of Welch and Flexner and many others have confirmed the orig- 
inal belief that the bacillus is a frequent excitant in man of a serious in- 
fectious disease, characterized by a local or widespread serous and em- 
phj'sematous phlegmonous inflammation, frequently associated with 
gangrene and general symi)toms of a profound toxaemia. 

The Bacillus aerogenes is rather large, on certain media spore form- 
ing, is often capsulated, and occasionally forms chains. It retains the 
stain by Gram's method. It is anaerobic, growing readily in a variety 
of artificial culture media. 

Babbits are not susceptible to even large intravenous injections of 
pure cultures. But if Ihey be killed soon after such inoculation, within 
a few hours, at room temperatures, an abundant development of gas 
occurs throughout the body. On the other hand, the subcutaneous in- 
jection of a very small quantity of the fresh oedematous exudate is fol- 
lowed by the typical local and general marks of infection. Guinea-pigs 
are more susceptible than rabbits to inoculation, either with cultures or 
fresh material, and develop characteristic lesions. 

While infection may occur without gas, in most cases before death 
and especially after, there is an abundant formation of gas in the tis- 
sues. This is largely hydrogen formed through the splitting by the 
bacillus of either sugar or proteids. While the gas may be present in 
any of the tissues, in the body cavities, and in the blood-vessels, it is 
especially in the liver after death that the marks of gas accumulation 
are most striking. This organ maj^ be riddled with small holes, present- 

' Critical summary and bibl., Netter, Arch, de Med. exp., t. xii., p. 86, 1900. 
- For studies on various forms of hsemorrhagic infection see Babes, Verh. d. deutschen 
path. Gesellschaft, Bd. ii., p. 262, 1900. 



244 THE INFECTIOUS DISEASES. 

ing an appearance which has been characterized as '^ foamy liver ^' (Fig. 
322, page 557). 

Infection may occnr through wounds or injuries in any part of the 
body. It has been frequently observed in pregnant and puerperal 
women. Ulcers of the stomach and intestine, or the urinary tract, may 
be portals of entry. One of the more common forms of local infection 
is the so-called gaseous phlegmon or emphysematous gangrene. Pul- 
monary and pleural lesions, appendicitis, and peritonitis are described 
as well as gaseous abscesses and purulent meningitis. While the usual 
action upon the tissues is the induction of bloody oedema and necrosis, 
this bacillus is also occasionally pyogenic. 

The natural habitat of the organism is the soil and the intestinal canal. 
This accounts for the relative frequency of infection through the intes- 
tinal and genito -urinary tracts and through wounds contaminated with 
dirt. 

Infection, especially from the intestinal canal, may apparently occur 
during the later hours of life, w ith or without symptoms and with a post- 
mortem formation of gas. It is often difficult to determine, since gas 
formation occurs so early and so extensively after death, whether the 
entrance has or has not been effected during life. It seems fair to infer, 
as the result of animal experiments, that when the gas formation, even 
after death, is widespread, ante-mortem infection had occurred. 

Concurrent infection with other organisms, especially the pyogenic 
cocci, is frequent. 

Welch and ^NTuttall early called attention to the importance of recog- 
nizing the possibility of infection with this bacillus in judging of a cer- 
tain class of cases of alleged air embolism. 

It is probable that the Bacillus aerogenes capsulatus is identical with 
forms which have been described under various names in connection with 
cases of gaseous phlegmon, or so-called malignant oedema.' 

Bacillus (Edematis Maligni. 

The bacillus of malignant oedema, which is frequently present in dust, in putrefy- 
ing substances, and in soil, considerably resembles the Bacillus aerogenes capsulatus both 
in its morphological and biological characters. It is, however, more slender, and more 
apt to form threads ; spore formation occurs readily in the ordinary media. It decol- 
orizes partially by Gram's method. Other diiferential characters are to be made out in 
cultures. It is an excitant of hsemorrhagic cedema in animals, but with slight if any 
development of gas. 

Other Bacteria which May Induce Hsemorrhagic Septicaemia. 

Nearly related to the Bacillus aerogenes capsulatus and to the bacillus of malignant 
oedema are several other spore- forming anaerobic bacilli occurring especially in tlie 
earth, in excrement, and in various rotting substances. Some of these appear to be of 
pathogenic significance in the lower animals under both natural and experimental con- 
ditions. 

1 For an excellent critical resume of this subject, with bibliography, see Welch^ 
Bulletin of the Johns Hopkins Hospital, vol. xi., p.' 185, 1900. 



THE INFECTIOUS DISEASES. 245 

Thus the Quarter-evil (Rauschbrand ; charbon symptomatique), especially in Europe, 
is a serious infectious disease of sheep, goats, and cattle. At the seat of infection, often 
in the legs, there is a haemorrhagic oedema with gas formation, the in vol ved region often 
becoming much swollen and black in color (" black leg "). The bacillus which is the 
excitant of this disease is known, and preventive inoculation has been practised. 

Howard has described a group of cases of Imraorrliagic septicoimia characterized by 
haemorrhages into the skin, serous membranes, and viscera, in which capsulated bacilli 
apparently related to the above-described bacillus of Friedlander (page 189) have been 
found. For the details of these cases and their relationship to other forms of septicaemia 
we refer to the original paper. ' 



HYDROPHOBIA. (Rabies.) 

Morphology of the Lesions. 

This is an infections disease occnrring most freqnently in the carni- 
vora, and especially common in dogs and wolves. 

The lesions are not constant nor are they characteristic. Though 
well marked in some cases, in othei^s they are but very slightly develoi^ed. 




Fig. 132.— Hydrophobia, Transverse Section of Small Blood-Vessels ix the Spixal Cord. 
Showing accumulation of leucocytes and proliferation of connective-tissue cells in the adventitia of the 



Changes, when present, are ai)t to be most pronounced in the medulla 
oblongata and pons, but they may be present in the si)iual cord. They 
consist of small haemorrhages, accumulation of leucocytes in the pen- 
vascular lymi^h spaces about the blood-vessels (Fig. 132) and around 
the ganglion cells, of thrombi in the smaller blood-vessels, and finally of 
chromatolysis of the ganglion cells. 

Eecently changes have been described in the intervertebral ganglia 

^ Hoimrd, Journal of Experimental Medicine, vol. iv., p. 149, 1899. 



246 THE INFECTIOUS DISEASES. 

and in the plexiform ganglia of the pneumogastric nerve, which, al- 
though not limited to rabies, are yet so frequently present as to be ap- 
parently of value in diagnosis. The lesions consist in degeneration or 
atrophy or destruction of the ganglion cells with a proliferation of the 
endothelial cells lining the capsule. ^ 

The Excitant of the Disease. 

While there is reason for believing that hydrophobia is due to the 
introduction into the body of some special form of mici'o-organism, and 
while the recent researches of Pasteur and others have brought to light 
many interesting and important facts regarding the general nature and 
distribution in the body of the infectious agent, nothing is yet definitely 
known about the particular organism which induces the disease. 

It is known that the infectious agent is in the saliva and salivary 
glands of rabid animals, and that it may be present in the saliva of the 
dog two or three days before the symptoms of the disease are manifest. 
It is not present in the blood, but seems to be especially concentrated in 
the central nervous system and particularly in the medulla oblongata. It 
is readily rendered inert by corrosive sublimate and other germicides. 
It resists cold even to — 20° C. but loses virulence after one hour's ex- 
posure to 50° C. 

Preventive Inoculation. 

^N'otwithstanding the total ignorance of the micro-organism concerned 
in inciting hydrophobia, his genius in wise experiment enabled Pasteur 
to establish a method for artificial immunization against the disease 
which has proved most beneficent. 

After obtaining a virus of high and definite intensity, which was ac- 
complished by a series of inoculations beneath the dura mater in rabbits of 
portions of the spinal cords of rabid animals, it was found that by dry- 
ing in the air, spinal cords of rabbits having definite and high virulence, 
with due protection against aerial contamination, the virulence dimin- 
ished day by day. With virus thus obtained of virulence ranging from 
that which is practically inert to that of the utmost potency, it has been 
found possible safely to accustom both animals and men to the presence 
of amounts of hydrophobia virus contained in the spinal cord emulsion, 
which under ordinary conditions would prove speedily fatal. In other 
words, it has been found possible to confer artificial immunity against 
the disease. 

This process occupies several days, and immunization must be com- 
pleted before the disease has begun to manifest itself ; but as the incuba- 
tion period in hydrophobia is a long one — the average is about forty days 
— it has been possible, in a large and increasing number of cases, to save 
the lives of persons bitten by rabid animals. 

^ See Bavenel and McCarthy, University Medical Magazine, vol. xiii. p. 766, 1901. 



THE INFECTIOUS DISEASES. 247 



Diagnosis. 

In view of the importance of diagnosis, in animals Avhich have died 
or have been killed under suspicion of rabies, the spinal cord, medulla, 
and ganglia should be saved. Portions of the fresh medulla in watery 
emulsion should, if possible, be inoculated beneath the dura mater of three 
healthy rabbits, and the development of rabic paralysis and other symp- 
toms awaited. This operation for diagnostic pur^DOses should be done 
only by one experienced in this subject. Other portions of the medulla 
and cord and the ganglia should be hardened in Orth's fluid and alcohol, 
and carefully examined for ganglion-cell lesions, for small perivascular 
accumulations of leucocytes, and for changes in the spinal ganglia. The 
existence of these in the medulla and cord of an animal suspected of rabies 
will go far toward confirming the suspicion. 

It is always wise not to kill suspected animals, but to keep them un- 
der observation in confinement. Eabies being always fatal, recovery 
from a susj^icious disease excludes it, so that further protective meas- 
ures may be clearly unnecessary. On the other hand, the carefully ob- 
served symptoms of a suspected animal may even in the event of a fatal 
termination afford valuable evidence. If the laboratory for diagnosis be 
accessible, it is well, if the suspected animal should die or be killed, to 
send the whole animal or the head cut off low down, packed in ice. Cold 
does not rapidly diminish the virulence of the rabic virus. If the mate- 
rial is to be transmitted for a long distance, the brain of the animal with 
the medulla, carefully removed to avoid contamination, may be sent in a 
sterilized bottle containing a mixture of equal parts of glycerin and water, 
which has been sterilized by boiling and cooled. 

TYPHUS FEVER. (Hospital Fever ; Spotted Fever ; Jail Fever ; Ship 

Fever ; etc.) 

This highly contagious, infectious disease has not, so far as we know, 
any characteristic lesion save the petechial skin eruption ; but after death 
the body may present lesions common to many of the infectious diseases. 

The body has a tendency to rapid putrefaction, and the Mood is often 
darker and more fluid than is usual in other diseases. 

The voluntary muscles may be the seat of waxy and albuminous de- 
generation. 

The hrain and its membranes may be congested ; the mucous memhmne 
of the pharynx and larynx may be the seat of catarrhal or croupous inflam- 
mation. 

Lungs. — There may be bronchitis, broncho-pneumonia, or hypostatic 
congestion of the lungs. The walls of the heart may be soft and flabby. 

The agminated nodules of the ileum, and the mesenteric nodes may be 
swollen. The spleen is often large and soft from hyperplasia. The kid- 
neys and liver are frequently large and pale, and the seat of albuminous 



248 THE INFECTIOUS DISEASES. 

degeneration. The nature of the infective agent in typhus is unknown. 
Several observers have recorded the finding of micro-organisms of one 
kind or another in tlie body during life and after death, but proof that 
anv of these are excitants of the disease has not yet been furnished. 



YELLOW FEVER. 

Lesions of the Disease. 

This infectious disease is without characteristic lesions save for the 
haemorrhages and pigmentation in the skin. Such other lesions as com- 
monly exist are those common to toxaemia. The following conditions 
are, however, frequently present after death : 

Eigor mortis is marked and occurs early. 

The brain and its meninges are usually congested. The skhi is of a 
yellow color from the presence of bile pigment, and may be mottled by 
ecchymoses. 

The heart is of a pale or brownish-yellow color. Its muscular fibres 
may be the seat of fatty degeneration. The lungs may be congested. 

The Stomach often contains a characteristic dark fluid, due to altered 
blood iDigment, similar to that which is vomited during life — black vomit. 
Its mucous membrane may be congested, softened, and is sometimes 
eroded. The intestines are dark-colored, often distended with gas, and 
sometimes contain blood. The liver in the earlier stages of the disease 
may be intensely congested. More frequently it contains but little blood, 
is of a light-yellow color, and the hej)atic cells show the changes of an in- 
tense albuminous degeneration, often much more marked than are found 
in any other disease except acute yellow atrophj" of the liver. Areas of 
focal necrosis may be present. The gall bladder is apt to be contracted. 

The spleen shows no marked changes. The Mdneijs present an in- 
tense albuminous degeneration. The tubules usually contain masses of 
hyalin material. 

The Excitant of the Disease. 

A^Tiile its mode of occurrence and the characters of its symptoms and 
lesions afford a strong presumption that yellow fever is an acute infec- 
tious disease, none of the various studies which have been made upon its 
etiology have as j^et revealed the presence of any micro-organism which 
can be confidently accepted as its excitant. ' 

' The various studies of Sternberg, who isolated a bacillus whicli he called "Bacillus 
X," and of Sanarelli, who found a bacillus which he named Bacillus icteroides, are the 
most noteworthy earlier contributions to the subject. 

A later study and references to the bibliography of this subject may be found in 
an article by Reed and Carroll, Jour. Exp. Med., vol. v., p. 215, 1900. 

For a summary of observations relating to the mosquito as a possible intermediary 
host of the infectious organism in yellow fever, see Reed, Carroll, and Agramonte, Phila. 
Med. Jour., Oct. 27th, 1000; also Jour. Am. Med. Assn., Februarv 16th, 1901. 



THE IXFECTIOUS DISEASES. 249 



VARIOLA. (Smallpox.) 

Smallpox is an acute, readily commiiuicable, infectious disease, es- 
pecially characterized anatomically by an inflammation of the skin which 
passes through a series of more or less distinctive phases of papule, vesi- 
cle, pustule, with a final drying of the exudate and necrotic tissue con- 
stituting the crust. 

Various phases of the exanthem are used to designate forms of the 
disease. 

Secondary lesions are diffuse suppurative inflammation of the skin, 
inflammations of the mucous membrane, haemorrhages in various parts of 
the body, and albuminous degeneration of the kidney, li^er, and spleen. 

The skin lesion shows in general at first circumscribed areas of in- 
flammation above the ends of the papilla:', with the develoi^ment of a fluid- 



Fig, 133.— a Smallpox Vesicle of the Skin. 

filled reticulum, so that vesicles are formed (Fig. 133). These at first 
contain a clear fluid, but by the gathering of pus cells the fluid becomes 
turbid and accmnulates to form a pustule. Hand-in -hand with these 
changes the papillae and adjacent layers of the corium may become infil- 
trated with cells. The contents of the pustules and the necrotic tissue 
above dry and form the crusts. AMien the changes are largelj' confined 
to the epidermis the lesion may leave no deformity. But if the changes 
in the cutis are considerable, cicatricial tissue may form, leaving scars. 
The association of local hsemorrhage with the above changes gives rise to 
the haemorrhagic form of exanthem. 

Various micro-organisms, both bacteria and protozoa,' have been 
described as occurring in the local skin lesions of smallpox, but the ex- 
citant of the disease is still unknown. 

The protection conferred by a successfully weathered attack of small- 
pox is one of the most striking examples of this form of acquired im- 
munity (see p. 170). The more recent view of the immunity conferred 
by vaccination against smallpox is based upon the demonstration that the 

' Consult Feed Jour. Exp. ]Med.. vol ii., p. 515, bibliog. ; also Hugnenin, Lubarsch 
and Ostertag's "Ergebnisse," Jahrg. iv., p. 387. 




250 THE INFECTIOUS DISEASES. 

disease variola in man and the disease vaccina in the bovine species are 
the same, and not different, as was formerly believed ; that the disease 
in the cow is only a modified form of the human disease. The effect of 
the passage of the unknown micro-organisms through the insusceptible 
bovine — thus runs the rationale in the new light — is so to diminish the 
virulence of the germ that by its subsequent inoculation in man immu- 
nity is secured without the profound disturbance which infection with a 
germ of unmitigated virulence would involve. ' 

SCARLET FEVER. (Scarlatina.) 

This is an infectious, readily communicable disease characterized by 
a diffuse skin eruption, and frequently accompanied by inflammation, 
either catarrhal, or croupous, or gangrenous, of the tonsils, pharynx, and 
larynx. Focal necroses, albuminous degeneration in the viscera, and 
leucocytosis may occur. 

There may be acute hyperplasia or suppuration of the cervical lymph- 
nodes. There is very frequently an acute exudative or an acute diffuse 
nephritis. The spleen may be enlarged. Broncho-pneumonia, endocar- 
ditis, and pericarditis may complicate the disease. 

The exanthem or skin eruption in scarlatina is a simple dermatitis, as 
the result of which the papillae and subpapillary stratum become infil- 
trated with fluid or leucocytes, or both, the leucocytes being gathered 
especially about the blood-vessels. There may be small haemorrhages, 
and the acute phase of the inflammation is followed by an increased pro- 
duction of epithelium and an exfoliation of the superficial layers. These 
lesions of the skin may be, excepting the haemorrhages, very slightly 
marked after death. 

That the disease is due to some form of micro-organism there can be 
no doubt. The exact nature of this organism is not yet known. The 
acute nephritis and the marks of degeneration and focal necrosis so 
often present appear to be due to some poison formed in the body during 
the disease. 

One of the most marked features of the disease is the predisposition 
which it entails to the incursions of pathogenic germs other than that 
which we believe to be its excitant. Thus an infectious croupous in- 
flammation of the mouth, tonsils, pharynx, larynx, and trachea, due to a 
streptococcus (see page 186), is a frequent complication. True diph- 
theria due to the Lofller bacillus is also prone to establish itself upon the 
vulnerable inflamed mucous membranes. So also the frequently asso- 
ciated pneumonia, the inflammatory hyperplasia and suppuration of the 
lymph-nodes, suppurations in various parts of the body, the endocarditis 
and pericarditis which are not uncommon, may all be due to a secondary 
infection with the pyogenic cocci. ^ 

' Consult for general bibliography Freeman, article on vaccination in " Cyclopedia 
of the Diseases of Children," vol. v., suppl., p. 263; or Moore, in "Twentieth Century 
Practice," vol. xiii. 

2 Consult for a study and bibliography Pearce, " Scarlet Fever, its Bacteriology and 



THE INFECTIOUS DISEASES. 253 



MEASLES. 



A readily communicable infections disease, the most prominent feat- 
ures of which are an intense hypereemia with inflammation of the skin, 
associated with catarrhal inflammation of the mucous membrane of the 
air passages. The inflammation of the skin is anatomically of the same 
general type as that in scarlatina. Albuminous degeneration of the kid- 
ney or acute exudative nephritis may occur. Focal necroses in the liver 
and kidneys have been described by Freeman. ' 

The more common secondary lesions are broncho -pneumonia, pseudo- 
membranous inflammation of the pharynx and larynx, suppurative in- 
flammation in various parts of the body, and diphtheria. These compli- 
cations, as in scarlatina, are doubtless, in part at least, due to secondary 
infection with other germs than those causing the disease itself. 

The excitant of measles is not definitely known. 

Canon and Pielicke in 1892 "^ recorded the discovery in the blood in fourteen cases 
of measles of ver}^ small bacilli, about as long as the radius of a red blood cell, 
but varying considerabl}^ in size. These bacilli were sometimes abundant, sometimes 
scanty in the blood, lying singly or in heaps. Meagre cultures were obtained in three 
cases in beef tea. They did not seem to grow on the ordinary solid media. Bacilli 
similar in form were found in the exudate from intiamed mucous membranes in measles, 
The observations of these writers are interesting and suggestive, but until they shall 
have been confirmed by others and been greatly extended nothing can be assumed as 
established regarding the etiological significance of the germs. 



WHOOPING-COUGH. (Pertussis.) 

Whooping -Cough is an infectious disease, often epidemic, without 
characteristic lesions. There may be an associated bronchitis or bron- 
cho-pneumonia. Several observers have isolated bacilli from the sputum 
in whooping-cough, but the proof that these are the excitants of the dis- 
ease has not been furnished.^ 



BERI-BERI. 

Beri-heri is a disease of warm climates, believed by some observers to be infectious 
in character, by others to be due to unsuitable diet. The lesions are often not well de 
fined. There are in some cases subcutaneous oedema and dropsy. There is often degen- 
eration of the peripheral nerves and of the heart and voluntary muscle. The bacterial 
studies which have been made upon beri-beri have not led to definite results.'* 

Gross and Minute Anatomy," Med. and Surg. Eeports of the Boston City Hospital, 1898 
and 1899. 

1 Freeman, Arch, of Pediatrics, February, 1900. 

2 Berliner klin. Wochenschr., April 18th, 1892. 

'^ Koijlik, Centralblatt fiir Bakteriologie, etc., Abth. i., Bd xxii., p, 222, 1897, 
Consult Walsh, " Contributions from the William Pepper Laboratory of Clinical Medi 
cine," 1900, p. 450, bibliography. 

■* For bibliography of beri-beri see Sodre, " Twentieth Century Practice, " Bd. xiii. 



252 THE INFECTIOUS DISEASES. 



ACUTE RHEUMATISM. 

While the excitant of acute rheumatism is unknown there is much 
reason to believe that it is an infectious disease. There are no charac- 
teristic lesions; but various joints are frequently the seat of slight exu- 
dative inflammation, serous or fibrinous in character. Albuminous de- 
generation of the visceral cells with hyperplasia of the spleen has been 
noted. The disease is not infrequently complicated by endocarditis or 
pericarditis, by exudative inflammation of the lungs or pleura. Various 
micro-organisms have been found in the body in acute rheumatism ; of 
these the pyogenic cocci have been most frequently isolated, but these 
are probably to be regarded only as excitants of the suppurative or 
other complications. It is possible that more than one form of infection 
is embraced under the designation rheumatism. ^ 



MALARIA. 
The Excitant of the Disease. 

The excitant of the disease long known clinically as malaria is a small 
animal parasite, the Plasmodium malar ice, which enters the red corpuscles 
of the blood and in the course of its development destroys them. The 
destruction of each cell is coincident with the maturation of its contained 
parasite, which segments into a variable number of spores, or, more 
properly, merozoites, a phenomenon which is also coincident with the 
clinical appearance of the chill and its accompanying rise of temperature. 

These parasites of the red cell are protozoa belonging to a special 
sub-group, the hcemosporidia. For purposes of description these hsemo- 
sporidia of human malaria may be classified into three species or types, 
each of which incites a different clinical form of disease and each of 
which also differs from the other types in its morphology. These tyx3es 
are the tertian, the quartan, and the sestivo- autumnal parasites. 

Tertian and Quartan Types. — If the blood of a patient suffering from 
tertian fever be examined shortly after a chill, a number of the red 
cells will be found to contain small, highly refractile, actively amoe- 
boid bodies which are the early forms of the plasmodia or merozoites. 
The latter often take the form of small rings surrounding a central clear 
space. This is especially well seen in stained specimens (Plate I., Figs. 
1-4). If the blood be again examined some hours later, these very small 
forms will have grown to a considerable extent, and small brown or black 
granules will be noted in the body of the Plasmodium. This pigment has 
a very rapid motion inside the body of the parasite. If the blood be ex- 
amined at intervals for forty -eight hours the organism may be seen to 

' For summary of the bacteriology of Rheumatism see Poynton and Payne, The 
Lancet, Sept., 1900, pp. 861 and 832; also Poynton, Practitioner, vol. Ixv., p. 22, Jan., 
1901. 



THE INFECTIOUS DISEASES. 253 

have grown so large as to occupy nearly the whole of the red cell (Plate 
I., Figs. 5-12), which becomes somewhat swollen and pale, the latter effect 
being due to the destruction of the haemoglobin of the cell by the para- 
site, which thus produces the pigment granules of melanin with which it 
is filled. At the end of forty-eight hours the pigment has collected in 
the centre of the organism, which has ceased its active amoeboid motion. 
Now small pale spots, which are the nuclei of the segmenting mature 
form, become easily visible (Plate I., Fig. 16), and finally the red cell 
bursts, and the small merozoites, each containing a nucleus, are set free 
to enter other red cells and to repeat the cycle in another period of forty- 
eight hours. A certain portion of the free merozoites are destroyed by 
the phagocytic leucocytes and other cells. The free pigment left after 
the segmentation of the mature forms is also collected by these phago- 
cytes. Thus after severe and prolonged attacks of malaria the leucocytes 
are frequently filled with pigment. 

The quartan organism goes through a cycle similar to that of the ter- 
tian, except that the time required is seventy -two instead of forty -eight 
hours. There are also a few minor differences in the morphological ap- 
pearance of the two organisms. Thus the small early amoeboid forms 
of the Plasmodium are much more active in their movements in the ter- 
tian than in the quartan. The pigment in the tertian is very fine ; in 
the quartan it is often in small blocks or rods and is much coarser 
(Plate I., Figs. 22-25). The mass of segmenting merozoites in the tertian 
organism is quite irregular in shape and contains from fifteen to twenty 
individuals, while that of the quartan is a regular rosette in shape and 
the merozoites average from six to twelve (Plate I., Figs. 26-28). 

-ffistivo-Autumnal Type. — The parasite of the sestivo -autumnal fever 
develops in the blood in much the same way as the other forms, with the 
exception that the amoeboid rings are, as a rule, smaller. The signet- 
ring shape is more marked, and the pigment is less abundant (Plate I., 
Figs. 31-34). Another peculiarity of this organism is that the develop- 
ment of the larger amoeboid forms takes place chiefly in the bone marrow 
and the spleen, while that of the tertian and quartan is to be seen in the 
blood. Thus as soon as the Plasmodium of the sestivo -autumnal type has 
grown sufficiently to occupy about one-fourth of the red cell, it disap- 
pears from the peripheral blood and can be found developing in the blood 
obtained by puncture of the spleen, or iijr fatal cases, from the bone mar- 
row (Plate I., Figs. 35, 36). In such preparations the mature pi asmodia 
may be found and the segmenting process followed (Plate I., Figs. 37- 
39). The organism is not as large as the tertian, as the segmenting form 
usually only occupies about one-half of the somewhat shrunken red cor- 
puscle. The number of merozoites formed is about fifteen. The time 
of the developmental cycle in the blood is forty-eight hours. 

In the blood of a patient infected with the sestivo- autumnal parasite, 
there are always found within a few days of the beginning of the dis- 
ease a moderate number of crescent -shaped bodies with pigmented centres 
and the remnant of a red cell about them (Plate I., Figs. 13, 41). They 



Description or Plate I. 

Hsematozoa of Tertian Malaria. 

Figs. 1 to 4. . .Small ring-shaped merozoites of tertian malaria; 2 and 3, multiple in- 
vasion of a single red cell. 
" 5 to 12 . .Amoeboid forms of gradually increasing size. 

Fig. 13 Large amoeboid form in which the pigment is beginning to collect as a 

preliminary to segmentation. 

" 14 Pigment still more clumped, and the pale areas representing nuclei be 

gin to be marked. 

" 15 .Segmenting form with an irregular mass of merozoites. 

" 16 More symmetrical type of segmentation with central block of pigment. 

17 Free merozoites after leaving the red cell. 

" 18 Gamete. 

" 19 Microgametocyte with flagella or microgametes. 

Haematozoa of Quartan Malaria. 

Figs. 20 and 21 . . Small ring form of merozoites. 

" 22 to 25. . . . Amoeboid forms with coarse pigment. 
" 26 " 28. . . . Segmenting forms. 

" 29 Gamete. 

" 30 Microgametocyte with microgametes in the process of formation. 

Haematozoa of -ffistivo-Autumnal Malaria. 

Figs. 31 to 34 . . Small ring forms, some of them on the surface of the corpuscle ; 32 and 

33, multiple invasion of the red cell. 
" 35 and 36, Amoeboid forms found in the peripheral circulation. 
" 37 to 39 . . Large amoeboid forms and segmenting parasites found only very rarely 

in the peripheral circulation, but abundantly in the spleen and bone 

marrow. 

" 40 " 42.. Young crescentic forms not found in the peripheral circulation, but 
chiefly in the bone marrow. 

" 43 and 44, Adult crescents or gametes, found abundantly in the peripheral blood. 
" 45 " 46, Microgametocytes becoming oval and preparing to give off microga- 
metes. 
Fig. 47 Microgametocj^te giving off microgametes. 



Pathology— Z^^/^//^/^ and Prudden. 



m 



20. 



27. 



"^ 



45. 



1f' 17. IS. 



19. 



Pioematozoa of Tertian Malaria. 






29. 30. 

Haeniatozoa of Quartan Malaria. 






% # 



Hcematozoa of Aesti.'o- Autumnal Malaria. 



% 



35. 36. 37 



^ 



THE INFECTIOUS DISEASES. 255 

are devoid of amoeboid motion. The exact nature of these crescentic 
bodies was quite unknown until very recently, when it was discovered 
that they are bodies with sexual capabilities, whose function seems to be 
the prolongation of the species in a cycle outside of the human body. It 
had long been known that certain of the large mature amoeboid forms of 
the tertian and quartan organisms and the crescents of the 8estivo -autum- 
nal species did not undergo segmentation into merozoites, but remained 
circulating in the blood. When, however, the blood containing these 
forms was examined in a fresh condition on a slide, and especially if the 
blood before being covered was allowed to remain in a moist chamber for 
a few minutes, changes could be seen to take place which have not been ob- 
served in perfectly fresh preparations. Certain of the mature organisms 
set free long, actively motile ilagella T^hich entered other mature forms. 
In stained preparations it could be seen that each flagellum contained 
some of the nuclear chromatin of the organism from which it arose, and 
that this flagellar chromatin united with the chromatin of the body which 
the flagellum entered. The crescentic forms under suitable conditions go 
through the same process, the male crescent giving off flagella, one of 
which in turn fertilizes another crescent of slightly different morphology. 

Evidently this is a sexual process, and its occurrence only in blood 
which has been drawn from the body suggested the i^robability that under 
ordinary circumstances it takes place outside the human host. The truth 
of this conjecture has recently been established, and the process of fertil- 
ization and maturation of the fertilized organism has been found to occur 
in the stomach of a particular genus of mosquito, the Anopheles, ^o 
other species of mosquito is capable, according to our present knowledge, 
of acting as host to the Plasmodium of human malaria, though the organ- 
ism which induces malaria in birds can develop in a mosquito of the 
genus Culex. Whether the Plasmodium can carry out its sexual cycle 
under other conditions than in the stomach of the Anopheles is as yet 
unknown. 

If an Anopheles bites a patient with malaria, the blood and its con- 
tained organisms is drawn into the stomach of the mosquito, the fla- 
gella are given off from the mature forms or gametes and enter other ma- 
ture forms and fertilize them. The fertilized organism goes through 
a complicated develoi^ment, and the resulting si^orozoite finds its way in 
the course of a few weeks to the salivary glands of the mosquito host, to 
be injected into the blood of the next person bitten. The sporozoites 
probably enter the red cells as the small amoeboid forms or merozoites 
already described. 

Having outlined the sexual type of reproduction we shall now look 
more closely at its phases. The details of the process of fertilization and 
the formation of the sexual cells which are capable of carrying on the 
cycle in the mosquito have been best observed in the sestivo -autumnal 
fevers, so that the stages will be here described in connection with the 
development of the crescent gametes. These crescents are formed chiefly 
in the bone marrow from the small ovoid, intracellular bodies, which can 



256 THE INFECTIOUS DISEASES. 

early in their development be distinguished from the ordinary amoeboid 
forms by their more abundant coarse pigment and oval outline. 

The adult crescents are quite constantly present in Avell- developed 
cases, and are often found in the blood after treatment with quinine has 
caused the disapj)earance of the amoeboid bodies, the power of resisting 
the action of drugs being much more marked in the crescents than in any 
other form of the Plasmodium. Two types may be distinguished, both 
of which begin as small amoeboid forms and gradually mature into oval 
or crescentic organisms. One of these, the microgametocytes, or the cells 
producing the male elements, develops and gives off the flagellum 
(microgametes) ; the other, the macrogametes (female elements), neither 
form nor give off flagella. According to Marchiafava and Bignami ^ the 
microgametocytes are distinguished from the macrogametes by the fact 
that in the former (the male form) the pigment is gathered in a fairly 
compact mass in the middle of the crescent, the chromatin is more abun- 
dant, and the entire body stains faintly ; while in the female form, the pig- 
ment surrounds the rather scanty nuclear chromatin in a ring form, the 
cell body stains deeply, and no flagella are given off. The crescents in 
the fresh blood show no amoeboid motion, and even the j^igment is mo- 
tionless. They are either crescentic in form with the pigment collected 
at the centre, or they may be spindle-shaped with somewhat scattered 
pigment, or finally short, thick ovoid bodies with pigment irregularly 
scattered or more frequently gathered into a ring about the nucleus. 
They are all contained in red blood cells (endoglobular), the faint rem- 
nant of the red cell often being seen as a delicate line stretching between 
the two horns of the crescent. 

The formation of flagella (microgametes) does not take place in 
the circulating blood ; it begins only after the blood has remained on a 
slide for a few minutes or has remained for some time in the stomach of 
the mosquito. These flagella, usually about four in number, bud out 
from the perii)hery of one of the microgametocytes, which has assumed 
a spherical instead of a crescent shape, and grow to a length of three to 
five times the diameter of the red cell. They are either pointed or bul- 
bous at their extremities, or they present swellings at irregular intervals. 
Their motion in warm-stage preparation is rather rapid, and they finally 
become detached and move about free in the serum (Plate I., Figs. 45, 
46, 47). The pigment during this process usually remains at the centre 
of the sj)herical microgametocyte and is actively motile, but in prepara- 
tions stained to show the nuclear chromatin, the latter may be seen to 
penetrate the flagella in the form of long thin rods which remain after the 
flagella become detached. The shell of the red cell in which the cres- 
cent has developed can rarely be seen in fresh jDreparations of the flag- 
ellate forms. These flagella penetrate the body of one of the macroga- 
metes present in the slide and fertilize it. 

This process, which we have followed in an artificial preparation, seems 

^ Other observers claim that the pigment in the male forms is scattered throughout 
the Plasmodium. 



THE INFECTIOUS DISEASES. 257 

necessary for the continuance of the race, and is normally carried out in 
the middle intestine of tlie mosquito of the genus Anopheles. The actual 
entry of the microgamete (spermatozoon) into the macrogamete has been 
observed by MacCallum' in a fresh blood preparation, but so far the 
l^rocess has not been traced in the stomach of the mosquito, though free 
microgametes have been seen. 

If a patient in whose blood mature crescents are j) resent is bitten by 
the mosquito, the parasites develop in the intestine of the insect, and at 
the end of two days the fertilized forms may be found adherent to the 
wall of the intestine as small pigmented oval bodies quite similar to the 
early forms of the crescents develoj)ing in the human bone marrow. Two 
daj s later, the ijarasites or oocytes are much larger and have a distinct 
capsule, while by the sixth day they may measure from 60 to 80 ,a in dia- 
meter. They contain numerous small particles which are nuclei due to 
the frequent division of the original nuclear material, and the capsule is 
much thicker. At the end of a. week the parasite contains a large num- 
ber of slender thread-like rods with pointed extremities, each one of these 
rods having nuclear chromatin. The iDarasite or oocyst projects through 
the wall of the intestine into the coelom cavity of the mosquito host, and 
when it ruptures these minute rods or sporozoites are carried by the 
lymph currents to the salivary glands from which they may be injected 
with the saliva when the female Anopheles bites another subject. 

Though the actual entry has never been observed, it is su^Dposed that 
the sporozoites, after entering the circulation of man, attack the red cells, 
and, as we have seen, become the small amoeboid forms described above. 
In two to three weeks the formation of the gametes takes place, and the 
crescent forms appear in the blood. 

That the infection of man in this way is possible has been abundantly 
proven by allowing mosquitoes infected with sestivo-autumnal organisms 
to bite healthy persons, who, after a period of incubation of about ten 
days, are seized, with an sestivo -autumnal type of fever, and the character- 
istic organisms, though not present i)reviously, are now to be found in the 
blood. The mature forms or gametes of the tertian and quartan fevers 
undergo a course of development very similar to that of the sestivo-autum- 
nal fever, and are derived from the blood of the infected patient by the 
female of the same genus of mosquito, the Anopheles (Plate I., Figs. 19 
and 30). The sporozoites find their way to the salivary glands of the 
mosquito and enter the blood of the person infected while the Anopheles 
is biting. These sporozoites then enter the red cells as the small amoe- 
boid forms and carry on the sexual cycle in the blood until either the 
tissues of the body finally overcome the parasite, or treatment with qui- 
nine destroys the merozoites by means of its toxic action on these imma- 
ture forms. 

' MacCallvm, "On the Hsematozoan Infections of Birds," Jour, of Exp. Med., vol. 
iii., 1898, p. 117. 
17 



258 THE INFECTIOUS DISEASES. 



The Lesions of Malaria, 



The characteristic lesions of acute malarial infection are found in the 
blood, the liver, spleen, kidneys, and brain. 

The alterations in the blood are chiefly confined to the diminution in 
number of the red cor]Duscles, due to their destruction by the parasites 
developing in them and to a reduction in the haemoglobin content of 
those which do not contain ijarasites. These changes are apparently due 
to some toxic agent, for which there is additional evidence in the poly- 
chromatophilia and granular degeneration of the body of the red cell so 
often jpresent in severe malarial infections. The evidence of some poison 
acting on the protoplasm of the red cell is found, not only in those cells 
in which the organism is develoi^ing, but is more abundant in those cells 
in which no plasmodia are present. 

The leucocytes show slight qualitative changes, there being usually 
present a relative increase in the large mononuclear cells. Pigmented 
leucocytes are often seen, and in very severe infections large macrophages 
loaded with pigment may be seen in the circulating blood. In severe 
cases the i^igment, which is derived from the haemoglobin of the blood 
corpuscle and forms the granules in the body of the parasite, may be 
found free in the general circulation, but is usually soon removed by 
the leucocytes and the phagocytic cells of the liver, spleen, and bone 
marrow. The brain in cases of pernicious sestivo- autumnal fever is often 
much congested, and the smaller capillaries may be filled with enormous 
numbers of the i)lasmodia in various phases of development ; there may 
also be small punctate hsemorrhages in the white matter. The deposition 
of the malarial pigment in the cortex may give to the latter a dark red- 
dish-brown color, or it may be almost black„ The spinal cord shows 
similar changes. 

The liver in acute cases may show focal necroses resembling those 
present in other infectious diseases. The endothelium of the liver capil- 
laries may contain much pigment (see Fig. 313, p. 543), while the lumiua 
of the capillaries may be stuffed with iilasmodia in various stages of de- 
velopment. The Mdneys may show albuminous degeneration, and while 
the intertubular capillaries may be filled with pigmented leucocytes 
there is not, as a rule, a great accumulation of plasmodia in the vessels. 
A moderate diffuse nephritis is occasionally seen. The capillaries of the 
mucosa of the stomach and the intestines may be filled with parasites in 
cases with choleraic symptoms, and there may be a considerable amount 
of necrosis in the epithelium of the mucosa of the intestines. The bone 
marrow usually contains large numbers of the plasmodia, chiefly seg- 
menting forms. A good deal of pigmentation is present, and an active 
phagocytosis is carried on, mainly by the giant- cell macrophages present 
in the marrow. Crescentic organisms may be present in the marrow 
even if these have not been iDresent in the blood during life. 

The spleen is increased in size, the pulp is softened and very dark, 



THE INFECTIOUS DISEASES. 259 

the Malpighian bodies are not well marked. Microscopically, the organ 
is gi^eatly congested ; many of the red cells are invaded by the plasmodia 
which are often in the segmenting stage. There is a A^ery active phago- 
cytosis by the macrophages present, often so extensive as to include the 
red cells with their contained parasites. 

In the chronic cases the patient may become extremely anaemic with 
nucleated red cells in the blood and a great reduction in the number of 
erythroblasts. The spleen is greatly enlarged, the capsule thickened and 
adherent to the surrounding tissues. The cut section of the organ is of 
a dark brown or slaty black from the deposit of pigment. The Mal- 
pighian bodies are well marked. The fibrous-tissue trabeculse are 
thickened, as is the reticulum of the pulp ; the pulp cells are pigmented. 
The liver shows a marked pigmentation, especially in the endothelium 
of the capillaries and in the so-called perivascular cells described by 
Kupffer, while occasionally there is a moderate amount of new connec- 
tive tissue, which, however, does not follow, as a rule, the anatomical 
distribution of the connective tissue in the usual atrophic cirrhosis. In 
chronic poisoning the kidneys may show a chronic diffuse nephritis. The 
bone marrow may remain fairly normal except for the deposition of pig- 
ment, or there may be seen a marked hyperplasia with replacement of 
the normal fatty marrow of the shafts of the long bones with red marrow 
containing normoblasts or even megaloblasts, if the disease has been long- 
continued and severe. ' 



Methods of Examination of the Blood. 

There are two methods of examinirig the blood for plasmodia, in fresh preparations 
and in stained smears. Both require considerable training, as the artefacts produced by 
imperfect technique have often been mistaken for organisms. 

The Examination of Fresh Blood. — To examine the fresh blood, a puncture is 
made in the pulp of the finger and a perfectly clean cover-glass just touched to the top 
of the drop of blood which exudes from the puncture. The cover is then dropped 
without pressure on a clean slide. The diameter of the drop on the cover-glass should 
never exceed 2 mm. , because if more be taken the corpuscles cannot spread out in a per- 
fectly thin layer, but ^'^ll overlap each other and the preparation will be useless. The 
search for the organism should be made with a one-twelfth oil-immersion lens and a 
moderate illumination. The organisms are best recognized by the actively motile pig- 
ment in the clear, highly refractile cell body. 

The Examination of Blood After Fixation. — If the examination cannot be 
made at once, stained preparations may be made. The smear should be made on a slide 
or large cover-glass. It is best fixed in a mixture of formalin and strong alcohol for 
one minute. The proportions are 2 c.c. of a ten-per-cent solution of formalin to 100 c.c. 
of strong ethyl alcohol. The organisms are most easily found and studied in prep- 
arations colored with thionin. The formula for the stain is 20 c.c. of a saturated solu- 
tion of thionin in fifty-per-cent. alcohol, added to 100 c.c. of two-per-cent aqueous so- 

^ A general bibliography of malaria to 1895 is contained in the excellent monograph 
of TMyer and Hewetson, "The Malarial Fevers of Baltimore," Johns Hopkins Hospital 
Reports, vol. v., 1895. The more recent literature, especially that relating to the de- 
velopment of the organisms in the mosquito, is in MarcMafava and Bignami, article 
"Malaria" in "Twentieth Century Practice," New York, 1900, and also Luhe, "Neuere 
Sporozoenforschung," Centralbl. f. Bakt., Bd. xxvii. and xxviii., 1900. 



260 THE INFECTIOUS DISEASES. 

lution of carbolic acid. The stain requires several days to ripen and then keeps indefi- 
nitely. Its action is rapid, requiring only about fifteen seconds to color the malarial or- 
ganisms deeply. 

To demonstrate the nuclear chromatin of the malarial parasites it is necessary to use 
special stains, the most useful being a modification of that originally devised by Roma- 
uowski for this purpose. ^ Two staining substances are necessary : (1st) a one-per-cent 
aqueous eosin solution; and (2d) a one-per-cent polychrome methylene blue solution. 
The latter is made by heating one-per-cent methylene blue dissolved in one-half per 
cent sodium carbonate solution to 55° C. for two days. At the end of this time certain 
decomposition products of the methylene blue are formed, which have the power of 
staining the chromatin of the Plasmodium. The staining mixture is made as required, 
by adding two to three drops of the eosin solution to 2 c.c. of water, then adding the 
polychrome blue, drop hv drop, until the red of the eosin is only faintly visible. The 
blood smear, which has been fixed in either ethyl or methyl alcohol, is laid face down 
in the mixed dye to prevent the precipitate from adhering to the preparation, and is 
left for from five to ten minutes. Wash in water, dry, and examine with an oil-im- 
mersion lens. 

THE INFECTIOUS DISEASES OF ANIMALS. 

The study of comparative pathology is of great and increasing importance, and 
already much light has been thrown on the nature of human diseases by the study of 
the diseases of the lower animals. 

While this is true of pathology in general, it is of especial significance in the study 
of the infectious diseases of the lower animals, not only as they occur spontaneously, 
but also in fields of experimental research. 

The scope of the book does not permit of a more than occasional reference to animal 
diseases, but the reader may consult : Nocard and Leclainche, " Les Maladies Microbiennes 
des Animaux," Paris, 1898, and Frieherger and Frohner, "Lehrbuch der speciellen Patho- 
logic und Therapie der Hausthiere," 1896. 

Consult also the files of Lubarsch and Osiertag, "Ergebnisse der allgemeinen Aetio- 
logie der Menschen- und Thierkrankheiten. " 



BIBLIOGRAPHY OF THE INFECTIOUS DISEASES. 

For a fuller treatment of the themes considered in this chapter the reader may con- 
sult among the larger works : 

Flugge, "Die Mikroorganismen," 1896. This is in many respects the best general 
work. 

Mace, "Bacteriologie," 1901. Has recent bibliography, especially the French. 

Among the smaller works may be mentioned: 

Muir and Ritchie, "Manual of Bacteriology," 1899. This is an excellent epitome. 

Abbott, "Principles of Bacteriology." Especially good as a working laboratory 
manual. 

Park, "Bacteriology in Medicine and Surgery," 1899. Presents certain hygienic 
and public-health aspects of the subject. 

Wurtz, "Precis de Bacteriologie cliuique." Summarizes the micro-organisms which 
have been found in various lesions. 

Hueppe. "Principles of Bacteriology." English translation by Jordan, 1899, is an 
admirable general treatment of the subject, based upon a scientific rather than upon 
the traditional conceptions of the relationships of bacteria to disease. 

LuMrsch and Ostertag's "Ergebnisse der allg. Aetiologie der Menschen- u. Thier- 
krankheiten " contains valuable resumes and bibliography, issued yearh\ 

A large part of the record of recent study is widely scattered in monographs and 
journals. 

^ NocM, Centralbl. f. Bakt., Bd. xxv., 1899, p. 764. 



CHAPTER IX. 

TUMORS. 

The Nature and Characters of Tumors in General. 

The word tumor, which was originally applied to any swelling, has 
become more and more strictly limited in meaning until it is now com- 
monly used to designate certain more or less circumscribed new tissue 
growths or neoplasms. But the formation of new cells and new tissues 
is of such common occurrence under normal as well as under various ab- 
normal conditions that it is desirable for us to fix if possible upon some 
features by which the tissue growths called tumors may be distinguished 
from other normal or abnormal new-formed tissues. In the first place 
tumors, like all tissues formed in the body after embryonic life, are pro- 
duced by the proliferation of cells of normal types, each of its kind. 

It would be well in this connection to remember that a given cell of 
whatever type, be it of connective tissue, muscle, gland, or nerve, can 
fully maintain the characters of its type only so long as the conditions 
of its life do not greatly differ from those under which by adaptation to 
environment the type was finally fixed. The characters of cells are 
largely shaped by heredity, and these characters are maintained with 
great tenacity, but both in form and function cells may be largely swayed 
by external influences. The marks of departure from the type in cells 
subjected to an unusual environment may be evident when expressed in 
form or structure, and sometimes in function, but it is well not to forget 
that even our most refined methods of study of cells leave by far the 
greater part of their metabolic performances Avholly in the dark, while 
we seem as yet to be only on the threshold of knowledge of their structu- 
ral details. 

These considerations are especially important in the study of tumors 
as of all new tissue formations, because the key to our understanding of 
these lies largely in the appreciation of the fact that every cell in the 
differentiated tissues comes from a cell of the same type. But this, 
which is sometimes called the principle of legitimate succession in cells, 
assumes that the conditions under which the life of the new cell is main- 
tained shall not depart too widely from the normal, that is, the usual. 
The bearing of this limitation will be evident as we proceed in our study 
of tumors. 

The capacity for cell proliferation is most marked in the embryo and 
during the earlier periods of individual life. When the body attains its 



262 TUMORS. 

develoi^ment, the power of cell reproduction, as we have seen — see Re- 
generation, p. 98 — is largely limited to special forms of tissues, such as 
connective tissue, the blood, and certain kinds of epithelium. This 
constant normal regeneration makes good the wear and tear of normal 
cell life. But here the capacity for multiplication in the cells is closely 
confined to the requirements of the body. A definite physiological con- 
trol is evident, similar in character to that under which in normal devel- 
opment the amount of new tissue is limited and its adaptation to the 
organism as a whole secured. 

Under normal conditions, furthermore, there may be a very large 
new formation of tissue under special physiological excitation, as in the 
mammary gland and the uterus in pregnancy. But here also the charac- 
ter and amount and the functional capacity of the new tissue are strictly 
limited and subservient to the welfare of the individual. 

Let us now turn from these normal new tissues to those which are 
abnormal. We have already seen, especially in our study of inflamma- 
tion, that new tissues may form even in considerable amount under 
abnormal conditions, such as injury with subsequent repair ; excessive 
functional activity as in various hyperplasise ; and under circumstances 
which involve a special and little understood persistent stimulus, as in 
interstitial inflammations. But under these various conditions also the 
tissue growth is local, typical in structure, usually limited in amount, 
and in most cases appears measurably to accord in nature and distribu- 
tion with the maintenance of the structural integrity and general welfare 
of the individual. The new tissue, in other words, maintains under all 
these varied conditions a definitely co-ordinated relationship to the body 
as a whole. 

While it is as yet imx^ossible to define tumors in such a way as abso- 
lutely to distinguish them from such other new tissue formations as we 
have just cited, they are in general characterized by such irregularity in 
growth both in structure and extent; by such a lack of relationship to 
the functional requirements of the individual, ' by such an independence 
of that subtle physiological restraint which limits cell growth and pro- 
liferation in the normal body, that their distinguishing character is per- 
haps best indicated by the word autonomy, or by the more striking sug- 
gestions of the term cell-anarchy. The autonomous or independent 
character of tumors, as has been very clearly formulated by Thoma, is 
especially manifested in the distinct limitation of the growth at the start ; 
in the tendency to variation in the structural type ; in various functional 
aberrations of the new cells ; in their interference by compression or 
otherwise with adjacent parts ; in their proneness to multiply through 
local or distant transplantation of cells ; and finally, in their liability to 
various forms of degeneration and necrosis. 

The reason why we cannot more accurately characterize tumors in 

^ An example of a certain phj^siological independence in tumors is seen in lipomata, 
in which a large amount of fat tissue may persist in an ill-nourished individual whose 
fat has otherwise almost wholly disappeared ; or in myomata of an extremely atrophied 
uterus. 



TUMORS. 263 

distinction from other new tissne formations is chieflj^ because we do not 
yet know what are their immediate excitants. To this subject we shall 
presently return, but we must first look at the general characters of 
tumors. 

Tissue Types in Tumors. — Tumors, as we have seen, are composed of the 
same types of tissue as those normally existing in the body, and from 
the latter they are derived by a proliferation of pre-existing cells. Thus 
tumors of the connective -tissue type originate in connective -tissue cells, 
of the epithelial-tissue type in epithelium, of muscle in muscle, etc. 

Tumors are not only analogous to the normal tissues of the body in 
structure, but their life history is manifested under the same general 
laws of nutrition, growth, reproduction, etc. Thej^ are supplied with 
blood-vessels which grow into them from adjacent healthy parts, just as 
these do, for example, into granulation tissue, so that they may finally 
possess a more or less independent vascular system of arteries, capil- 
laries, and veins. They have lymph-vessels and some of them nerves. ^ 

While the cell divisions by which tumors grow exhibit in general the 
same minute iDhenomena as does cell division in normal tissues (see page 
95), abnormal mitosis is frequent. Thus it may be multipolar; the 
chromatic substance may present great irregularity in form and amount 
(Fig. 30, page 97) ; there may be incomplete nuclear division, or the new 
nuclei may vary in size and form. While all these abnormalities may 
occur in the new tissue formations and may be experimentally incited, 
they are unusually frequent in certain tumors and mark one of the ways 
in which the lawlessness of tumor growths is manifested. 

Degenerative and Destructive Processes in Tumors. — Tumor tissues are 
subject to the same degenerative changes as other tissues; they may 
become fatty or calcified, ulcerated, gangrenous, pigmented, etc. By 
necrosis a tumor may be largely destroyed, though complete obliteration 
rarely occurs in this way. They are liable to undergo the ordinary in- 
flammatory changes, granulation tissue may form in them, and abscesses 
and cicatrices, a 

The rapidity of growth of tumors varies greatly; some grow very 
slowly indeed and may change but imperceptibly in size and appearance 
for years, while others grow so fast that they do not acquire solidity, and 
their elements remain in an incompletely developed condition and are 
thus more liable to destructive changes than are normal tissues. In 
healthy tissues the blood-vessels are supported by surrounding elements, 
which aid them in sustaining the blood pressure from within. In rap- 
idly growing tumors this external support is often lacking, and, as the 
walls of the blood-vessels are themselves often badly formed, the result 
is that the walls are apt to become pouched or aneurismal, and they often 
burst, giving rise to larger or smaller interstitial haemorrhages. 

Shape, Size, and Modes of Extension of Tumors. — Tumors have various 
shapes: nodular, tuberous, fungoid, ]3oly]3oid, papillary, dendritic, etc. 

^ For a study of nerves in tumors see Young, Jour. Exp. Med., vol. ii. , p. 1, 1897, 
bibliography. 



264 TUMORS. 

Tumors may occur singly or in greater or less numbers in the same or 
in different parts of the body. If they be multiple they may have oc- 
curred simultaneously or at different times as independent structures. 
Or, multiple tumors may occur as the result of the dissemination in the 
body, from a primary tumor, of cells which form a stai^ting-iDoint for 
new tumors. Many tumors are sharply circumscribed, may be even en- 
capsulated, and inflaence surrounding parts only by the pressure which 
they exert upon them. In this way they may cause displacement, atro- 
phy, or necrosis; they may, by pressure on neighboring vessels, induce 
oedema, thrombosis, etc. ; they may in the same way lead to dislocation 
and caries of bones. 

Tumors may grow largely by increase of elements within them, thus 
simply exiDanding; this is called central growth. They may grow in part 
or largely at the surface — peripheral growth. In this case the growth may 
be a direct, continuous enlargement of the mass at or near the periphery, 
or it may be by the formation of secondarj^ nodules near the primary 
growth, which, gradually enlarging, finally coalesce with the latter, 
forming a part of the nodular tumor. This mode of enlargement is 
Q'^Wq^ discontinuous peripheral growth, and is due to the dissemination of 
cells from the mother tumor into the adjacent tissue through the blood 
01' lymph channels, and their proliferation at the points of lodgment. 
This dissemination may occur by the agenc}^ of blood or lymph currents 
or by the amoeboid movements of the cells. Those new cells formed in 
tumors which are characteristic of the growth are all descendants of the 
cells in which the neoplasm starts and maintain their general type. But 
the old tissue of the part in which the tumor grows may remain with its 
vessels and form a matrix whose interstices are filled with the new tumor 
tissue ; or, the old tissue may furnish the starting-iDoint for a new growth 
of a fibrous and vascular nutrient and sustaining stroma. 

Metastasis of Tumors. — All tumors are not limited, as we have seen, to 
that i)art or region of the body in which they first occur. Sooner or later 
secondary nodules resembling the first may be found in distant parts of the 
body, sometimes singly, sometimes in great numbers. These may grow 
like the parent tumor, and themselves form foci for new disseminations. 

This dissemination of tumors is one of the most important elements 
of malignancy, and is called metastasis, the secondary tumors being called 
metastatic tumors. This occurs by the transportation of tumor cells 
through the blood or lymph channels. Since the tumor itself may con- 
tain new and badly formed blood and lymph vessels, and its structures 
be in close contact with the vessels of the tissue in which it grows, the 
cells of the primary tumor may, by ulceration through or by atrophy 
of the walls, readily find their way into the lumen of the vessels and be 
swept away by currents as emboli, and, finding lodgment, proliferate 
and grow, forming secondary tumors ; or the proliferation may occur in 
the vascular endothelium itself, when the formation of emboli is easy to 
understand. When carried through the lymph vessels the tumor cells 
may for some time be kept from the larger channels and from general 



TUMOKS. 265 

dissemination by lodgment in the lymph-nodes, where they may estab- 
lish independent tumors. 

The tumors in which metastasis is most apt to occur are, as a rule, 
those which grow rapidly, are vascular and succulent, and contain many 
cells. The parts of the body in which metastatic tumors are most apt to 
form depend, of course, upon the situation of the primary tumor and the 
distribution of the vascular channels through which dissemination occurs. 

Metastasis affords one of the most noteworthy examples of the great 
proliferative capacity of the cells of malignant tumors. For in the me- 
tastasis of normal tissue cells, such as not infrequently occurs after inju- 
ries to the bones or the liver, for example — the so-called parenchyma 
cell emboli — the transported cells iilvariably soon die and are disposed 
of as foreign bodies. But the exalted x)roliferative capacity of detached 
tumor cells enables them in spite of adverse conditions to establish and 
maintain fresh foci of vigorous tissue growth. 

The Malignancy of Tumors. — Kot less variable than the size, mode of 
growth, and structure of tumors is their significance in the organism. 
It is customary to classify tumors, for practical j^urposes, as malignant 
and benign, and for a long time malignant tumor and cancer or carcinoma 
were synonymous terms, ^ow we know that other tumors as well as car- 
cinomata are malignant, and, furthermore, contrary to the former belief, 
that malignancy does not depend upon any specific extracellular agent in 
the tumor. By the malignancy of a tumor is not meant merely the grav- 
ity of its presence, for a simple fat tumor, by pressing on the trachea, 
may lead to suffocation, and any tumor may secondarily cause death by 
haemorrhage. The real elements of malignancy in a tumor are: 1. 
Invasion of adjacent tissues by eccentric or peripheral growth. 2. The 
tendency to local recurrence after removal. 3. The formation of metas- 
tases. 4. An interference with the nutrition and general well being 
of the body, which may give rise to a condition known as cachexia. 
The modes of invasion of surrounding tissues and the formation of me- 
tastases have b^n considered above. The tendency to local recurrence 
after removal is probably, in most cases, due to the incomi)lete removal 
of the peripheral infiltrating cells. These may be ^ ery few in number 
and lacking in characteristic structural features, but are none the less 
endowed with the caijacity of proliferation and development into a new 
and similar tumor at or near the seat of the one extirpated. The infil- 
trating peri]3heral cells may remain dormant for a long time after an 
operation, or may immediately commence to grow. But the mere fact 
that a second tumor develojDS in the j)lace of one removed does not imjDly 
malignancy, since this may result from a continuance of the conditions 
which induced the first. 

The drain upon the system by the rapid growth of a tumor, together 
with the absorption from it into the body of deleterious putrefactive ma- 
terials, from sloughing, ulceration, and degeneration, or the occurrence 
in it of local infection with various micro-organisms may give rise to 
fever and other constitutional disturbances. Or, the tumor may induce 



266 TUMORS. 

feebleness, anaemia, and that general impairment of the nutritive func- 
tions of the body known as cachexia. This condition is frequently ren- 
dered worse by the mental status of the patient in the presence of such 
a traditional object of alarm. 

It should be remembered, however, that so long as they are localized 
and have not undergone degenerative changes, even the most malignant 
tumors do not usually give rise to a cachexia, since the drain upon gen- 
eral nutrition by their simple growth is not, under ordinary conditions, 
very great. When the system is deteriorated by the absorption of septic 
materials from tissue degeneration, however, this may become a very 
imi3ortant factor. 

This condition of cachexia, so evidently secondary to the growth and 
degeneration of the tumor, was formerly termed a dyscrasia or diathesis, 
and was supposed to precede and induce the growth of malignant tumors, 
particularly cancers. 

It is further to be noted that the fragments of tumors which have 
found access to the vessels may act as simjile emboli leading to immediate 
death, or, if infected, may incite metastatic abscesses. 

It was formerly supposed that the cells of malignant tumors, particu- 
larly of carcinomata, had a characteristic structure and appearance, and 
that by the examination of single or of a few separated cells the nature 
of the tumor could be determined. From the above considerations it 
will be evident, since all tumor cells have their prototypes in the normal 
body, that there is nothing pathognomonic in the ai)pearances of single 
cells. It is by a study of the general structure and of the topography 
of tumors, as well as of the characters of the individual cells, that we are 
enabled to determine their nature. And even then we must often bring 
to our aid the clinical history and gross appearances of the growth be- 
fore a definite conclusion can be reached. We may indeed sometimes, 
aided by the clinical history or gross appearances, be able, by the micro- 
scopical examination of scrapings from a tumor or of fluids from an 
internal cavity in which it is growing, to form a reasonable conjectui:e 
regarding its nature. As a rule, the peripheral portions of the more 
rapidly growing tumors are best adapted for microscopical examination, 
because here secondary degenerative changes are less likely to have oc- 
curred than in the central parts. 

The Transplantation of Tumors. — In view of the frequency with which 
fresh foci of tumor cell growth are established in the same individual by 
metastasis, by transplantation over serous surfaces, or on apposed mucous 
membranes, and stimulated by the few recorded cases in which tumors 
seem to have been incited in another individual through transference of 
the cells by contact, it is not surprising that a great deal of experimental 
work has been done upon the artificial transference of tumors by various 
forms of grafts or transplantations from man to the lower animals and 
from animal to animal both within and without the limits of species. 

The scope of this work does not permit a review of these interesting 
researches. But it may be said in general that they have been almost 



TUMORS. 267 

always unsuccessful save in a very few instances, within the limits of the 
same animal species, and even here the new growths at the seat of trans- 
plantation have been usually transitory or of doubtful character. The 
transferred tumor tissue is usually absorbed as foreign bodies commonly 
are, and the new tissue growths which have been not infrequently de- 
scribed are apparently for the most part of inflammatory nature. 

We are forced in all these exi^eriments to recognize subtle physiologi- 
cal conditions peculiar to even closely related species of animals without 
which their cells cannot flourish or long exist. Grafts of healthy tissue 
from individuals of the same species, especially of epithelium, may in- 
deed, as is well known, grow for a time and form foci of abundant new 
cell production ; but in such cases the new tissue is strictly subordinated 
to the ijhysiological requirements of the host and does not assume the 
characters of an autonomous neoplasm. ' 



The Etiology of Tumors. 

The etiology of tumors is one of the most complex and in many ways 
difficnlt subjects in general pathology, and with the limitations which 
the character of this work imposes we can touch only briefly upon some 
of its more important aspects, referring to more extended works and to 
monographs for a vast amount of statistical and experimental data, as 
well as for the many more or less plausible hypotheses which have been 
framed in the attempts to comprehend these anomalous manifestations 
of cell energy. 

General Conditions. — We shall first consider some of the general con- 
ditions which seem to have a bearing upon the occurrence of tumors. 

Age. — AATiile it may be said in general that tumors are most frequent 
in adult and advanced life, it is noteworthy that tumors of the connective- 
tissue type are apt to develop earlier, while the epithelial tumors are 
more frequent in the later periods. Thus, in one thousand and sixty- 
three cases of ^ithelial tumors analyzed by Gallard, only six occurred 
in the first ten years of life. The most common situation of tumors dif- 
fers also in the young and in the old. Thus, in the earlier years, as 
statistics show, the most frequent seat of tumors is the eyes and their 
adnexa, the kidneys, bones, and testicles ; whereas in adults and the aged, 
the stomach, uterus, liver, and mamma are most commonly involved. 

Sex. — Sex is also a significant factor in the development of tumors, 
especially of those which are malignant. Thus, in general, it may be 
said that the statistics indicate malignant tumors to be about twice as 
frequent in females as in males. This proportion, however, does not hold 

^ The results of experimental transplantation of tumors have been well summarized 
— with bibliography — \}j Menetrier in Bouchard's "Traite de Pathologic generale," vol. 
iii., Partii., p. 752; also by Sailer, Am. Jour. jNled. Sciences, vol. cxx., p. 190, 1900, bibl. 
See further Nichols, Jour. Boston Soc. Med. Sciences, vol. v., p. 34, 1900. Consult also 
for the results of the transplantation of embryonal cells in the adult animal's body, 
Birch- Hirschf eld and Garten, Ziegler's Beitrage, Bd. xxvi., p. 132, 1899, bibliography. 



268 TUMORS. 

good for tumors of the individual organs. For example, tumors of the 
stomach and of the tongue and lips are more frequent in men than in 
women. On the other hand, tumors of the breast are far more common 
in women than in men. 

Heredity. — While the influence of heredity is difficvilt to estimate ac- 
curately, there are a few well -authenticated instances of the remarkable 
prevalence of malignant tumors in families within a few generations. 
The general facts, however, are not so striking. The statistics of Wil- 
liams showed that in two hundred and thirty-five cases of carcinoma of 
the uterus or breast, about nine per cent, gave a history of carcinoma in 
father or mother, while in nearly twenty per cent, there was evidence of 
carcinoma in the family. In the estimates of other observers, the hered- 
itary influence seemed evident in about one -third or one -fourth of the 
cases. It is, however, instructive in this connection to note that in a 
study by Snow, of seventy-eight healthy persons there was evidence of 
carcinoma in the family in about one-fifth of the cases. 

It is clear, therefore, that while such statistics are suggestive and on 
the whole indicate that an hereditary iDredisposition to the development 
of tumors may exist, this does not in any way account for the immediate 
incitement of the growth of tumors, and is indeed, as Menetrier has urged, 
but one of many examples of hereditary predisposition which is observed 
in many forms of disease, sucli as infections, cerebral apoplexy, etc. 

The influence of climate^ food, race, and socicd condition has been in- 
voked as bearing upon predisposition to the growth of tumors ; but the 
evidence is not convincing that these are very significant in etiology. 

Local Predisposing Factors. — When we turn from the general to the local 
conditions bearing upon the origin of tumors, we find an imposing array 
of instances in which tumors, and especially malignant tumors, follow 
local injuries, either mechanical or toxic, or are associated with chronic 
inflammatory processes. Bruises or contusions, particularly those in- 
volving the bones, are not infrequently followed by malignant tumors, 
and it is noteworthy that these tumors are most apt to be of the connec- 
tive-tissue type — sarcoma, osteosarcoma, chondroma, etc. Epithelial 
tumors, on the other hand, are more frequently developed at the seat of 
repeated injury or long-continued irritation. Thus, epitheliomata are 
common in the mouth, near a rough ulcerated tooth, on the lips of pipe 
smokers, at the edges of chronic ulcers, on the skin of workers exj^osed 
to various chemical or mechanical irritants ; in cicatrices ; at the orifices 
of the stomach and at the anus. Finally, the frequent occurrence of car- 
cinoma of the liver with cirrhosis, though less easy of interpretation than 
many instances of the association of tumors with chronic inflammation, 
is worthy of notice in this connection. 

Before concluding this brief survey of the relationships of tumors to 
trauma, prolonged irritation, and chronic inflammation, ' it may be wise 
to remind the reader that undue significance should not be attached to 

' For an interesting study of the relationship of trauma to malignant tumor forma- 
tion see Broscli, Virchow's Arch., Bd. clxii., p. 32, 1900, bibliography. 



TUMOES. 269 

this occasional association, since in the great majority of cases these 
conditions are not followed by tnmors, nor, furthermore, has it ever been 
possible to induce genuine tumors experimentally under these readily 
secured conditions in animals. The bearing of trauma upon the origin 
of tumors is to be held in mind in estimating the influence of sex, since 
males are in general more liable to injuries than females. 

The relatively common develoiDuient of tumors in pigmented and 
other n?evi of the skin illustrates the significance of local mcdformations 
as predisposing factors in the origin of tumors. ^ 

Several cases have been recorded in which through injury there has 
been a mechanical displacement of cells — heterotojna — from which in 
their new situation tumors have dcAxloped. These cases, which have 
been in a measure paralleled by experiments in animals, illustrate an 
imi^ortant class of congenital tumors, often cystic in character, which 
arise from embryonal cell displacement, or, as is the case in many of the 
tumors of the neck at the site of the branchial clefts, from an imperfect 
closure of embryonal openings. 

We have seen that such evident malformation as the naevi of the skin 
may form the starting-point of malignant tumors. We know that in 
many cases cells or tissues or parts of organs displaced during embryonal 
life, as in the branchial clefts or in the kidney, may later develop into 
tumors. Cohnheim has gone further than this and framed an hy]3othesis 
to the effect that all true tumors are due to faulty embryonal develop- 
ment. In accordance with this hypothesis, cells which in the course of 
the development of the body may be displaced or become superfluous or 
do not undergo the usual changes, may remain for long periods unaltered 
but liable in later life, from whatever reason, to commence growing with 
all the potencies of lowly organized cells in the midst of the mature tis- 
sues. The noteworthy influence of heredity in the occurrence of some 
tumors, the congenital nature and early develoxDment of others, their 
atyi^ical structure in general, and the tendency of many forms to occur 
in situations in which during the development of the embryo consider- 
able complexity^exists, as well as their frequent jDrimary multiplicity — 
all of these characters of tumors lend considerable plausibility to Cohn- 
heim's hypothesis, and it appears to be applicable in certain cases. But 
it still lacks a morphological basis, since no one has seen the postulated, 
strayed, or dormant embryonic cells ; again, it by no means follows be- 
cause tumors often develop at the seat of malformations or may arise in 
embryonal heterotopias that all tumors are thus associated ; and finally, 
the frequent origin of epitheliomata in cells which have been formed in 
adult life, in cicatrices, for example, is evidence that this hypothesis is 
not in any event of universal application. 

' It should be remembered that many of the complex tissue groAvths often reckoned 
among tumors and called teratomata are really embryonic rudiments of another indi- 
vidual. While such rudimentar}^ embryos ma}^ be large and present such diversity and 
arrangement of tissue as to render the chaiacter of the growth obvious, they may, on 
the other hand, be very simple in character, as in some of the so-called dermoid cysts. 
These are all to be regarded rather as malformations than as genuine tumors. 



270 TUMORS. 

We have now reviewed a series of conditions whicli appear more or 
less directly to bear npon the origin of tnniors ; general conditions, such 
as age, sex, hereditary influences, etc. ; local conditions, such as congen- 
ital or acquired malformations, injuries, long continued irritation, or 
inflammatory processes. But when all these are taken into the account, 
we do not appear to have gained a definite clew to the immediate actual 
excitant of the new growths. Given any or all of the varied predispo- 
nants, why do the cells, which under any of these favoring conditions 
may have remained long inactive, and indeed usually do so, presently 
begin to proliferate and continue this new activity beyond the limita- 
tions of structural types or j)hysiological correlation'? It would appear 
that either there are external excitants of cell growth, as yet unknown to 
us, which suddenly become active, or else we are face to face with the 
fundamental problem as to the nature of the normal physiological im- 
pulses to cell growth and proliferation' and the restraining influences to 
which these are subject. 

Micro-organisms as Excitants of Tumors. — It is not surprising that 
micro-organisms should have been thought of as possibly direct excitants 
of tumors, especially in view of a certain crude analogy between some 
phases of tumor growth and metastasis and some forms of infection with 
metastasis. Bacteria of many kinds have in fact been frequently found 
in tumors of many sorts; but there is, in the opinion of the writers, no 
conclusive reason at hand for the belief that they are ever of any signifi- 
cance save as chance contaminations of vulnerable tissues or as incitauts 
of secondary and complicating lesions. 

A great deal has recently been written about certain structures which 
are not infrequently found in or between tumor cells, especially in the 
carcinomata, and have been hastily assumed to be parasites. These cell 
''inclusions^' are for the most part larger or smaller rounded bodies (Fig. 
134); with or without nuclei; sometimes with double contours, some- 
times not ; usually sharply outlined against the cell protoplasm in which 
they lie ; often crowding the nucleus to one side, often situated within 
the nucleus, or apparently replacing it. Some of them are invaginated 
epithelial or other cells, or cell nuclei which have undergone various 
degenerative metamorphoses, fragmentation, etc. ; some of the question- 
able structures appear to be the metamorphosed nuclei of the tumor cells 
themselves. They may be single or there may be several in a cell. 
Similar objects are to be found in other than tumor tissues. They are 
readily stained, with varying degrees of intensity, by hsemotoxylin, eosin, 
safranin, or fuchsin. There is in the writers' opinion no evidence either 
that these are living organisms or that they have anything to do with the 
origin of tumors. 

While coccidia or allied organisms with which these bodies have been 
compared are capable of inciting the growth of a small amount of new 
connective tissue and sometimes of epithelium, such growths are appar- 
ently inflammatory in character as are those other new tissue formations 
1 Consult the section on Regeneration, p. 94 



TUMOES. 271 

incited by the tubercle bacillus, the lepra bacillus, etc., which have 
sometimes beeu classed with tumors and called infectious granulomata. 
The reader is referred to the sections dealing with the nature of the 
inllammatory process in general, page 123, and to the introductory section 
in the present chapter for a review of the differences in the conception 
of the inflammatory i^rocesses and tumor formation. 

Attention has recently been called, in connection with tumors, to cer- 
tain forms of yeasts or blastomycetes as excitants of new tissue growths, 
but these also appear to be inflammatory. The cultivation of yeasts from 
the tissues of malignant or other tumors is of no more significance than 
the cultivation of bacteria under similar conditions. 

The nearly uniform failure in the attempts to transplant tumors from 
one species of animal to another, and the absolute failure to cultivate. 







Fig. 134.— Epithelial-Cell "Inclusions" in Tumors. 
Showing various forms. From carcinoma. 

either directly or by inoculation, any constant organisms from them 
which are capal^le of inducing experimental tumor growths, speak with 
much force against the notion of the parasitic origin of malignant tumors. 
Moreover, the great diversity in character and in the inconstancy of oc- 
currence of the objects which have been regarded as of possible signifi- 
cance in tumors, greatly diminishes the plausibility of the claims which 
have been made for them. 

It is much to be regretted that most of those who advocate the para- 
sitic nature of tumor excitants should be so engrossed with the alleged 
parasites that they largely ignore the dominant characters and the life 
history of the tumors themselves, especially of malignant forms, and the 
fundamental distinctions between these and such inflammatory growths 
as may superficially resemble tumors and which are undoubtedly often 
incited by various kinds of micro-organisms. 

We do not of course assert that tumors cannot be incited by parasites, 



272 TUMORS. 

but at present it seems to us that no adequate ground exists for believing 
that they are.' 

It is indeed not improbable that a local predisposition to tumor 
formation akin in nature to that which now and then is attributable to 
trauma may be occasionally induced by micro-organisms. But this it 
remains for future researches to demonstrate. 

The Complexity of the Problem of the Etiology of Tumors. — It seems to 
the writer that to seek for a single external excitant or group of ex- 
citants for the aberrant tissue growths which we call tumors is to ignore 
the many still obscure influences which are at work in all tissue growth, 
especially those physiological agencies which foster cell proliferation and 
tend, under the influence of heredity, to specialization in form or func- 
tion. On the other hand, not to be ignored are those influences, whether 
of nutrition or iDressure or exposure, which mould the cell growth under 
normal conditions into fixed and useful forms. It is rather a matter for 
surprise that ever-changing, self- regenerating living tissue does not 
oftener go astray in its activities than that it should only now and then 
do so. This latter somewhat inverted point of view may be useful in 
calling away the attention, in discussing the etiology of tumors, from a 
too close regard to extraneous factors, and directing it to the many still 
unexplored fields in cell iDhysiology with which we must perhaps become 
familiar before we can with fair hojDe of success attack the serious i^rob- 
lems of both the excitation and the prevention of tumors. 

No adequate conception can be gained of the complexity of the prob- 
lem involved in the origin of tumors or of the directions in which the 
highest promise of experimental research lies without a recognition of the 
new cell lore derived from a study of the lower and simpler forms of life.'^ 

The more commonly accepted and time-honored view of the imme- 
diate excitation of tumors is that they are due to some stimulus — ^^forma- 
tive stimulus " — by which the proliferative capacity of the cells is in- 
creased. What the nature of this postulated stimulus may be and how 
it is brought to bear upon the transformations of energy which through 
the subtle mechanism of the cell is manifested in proliferation, is in 
nowise clear, nor does it seem likely to become so until we gain a deeper 
insight into the life processes of the cell in general. It is possible that 
recent experiments (referred to on page 106) on the artificial excitation 
by chemical substances of cell proliferation and the development of the 
embryo in certain of the lower animals may lead to a wider conception 
of the nature of the conditions under which tumors are formed. 

There are obvious alterations in the character of the cell growth in 
tumors in which they deviate often widely from the norm. It has been 

' For bibliography relating to the alleged parasitic excitants of tumors, consult 
Gilchrut, Johns Hopkins Hospital Reports, vol. i., p. 332, 1896; also- Park, American 
Journal of the Medical Sciences, vol. cxv., p. 516, 1898. For an interesting resume of 
the factors involved in the origin of tumors see Adami, vol. vii., pp. 309 and 343, 1901, 
or Brit. Med. Jour., March 16th, 1901. 

■^ For a clear and comprehensive summary of the new lines of research in cytology, 
see Wilso7i, "Some Aspects of Biological Research, " The International Monthly, July, 
1900. 



TUMORS. 273 

suggested by Hausemann ' and others that these alterations may be due 
to a loss of differentiation in the tumor cells and the assumption of a 
more independent existence. This condition has been called Anaplasia, 
and while the term characterizes an important series of facts, it leaves 
them unexplained. 

Thus it is still uncertain whether the removal of mechanical or other 
restraints to cell growth and proliferation ; or the acquirement of new 
capacities through retrograde differentiation or reversion ; or the action 
of some as yet unknown "formative stimulus," are, either individually or 
collectively, and if so in what degree, concerned in the origin of tumors. 

A more subtle aud perhaps more comprehensive view of tlie agencies which must 
be taken into the account in the excitation of tumors is that especially advocated by 
Weigert'-^ and Ribbert.^ These observers and those in sj-mpathj^ with their views do 
not admit a new formative stimulus into their conception of the origin of tumors, but 
regard the usual potencies of the cells in this respect to be sufficient if the natural re 
straints to over proliferation be in any way diminished. 

Ribbert has perhaps more definitely than any other framed a working hypothesis 
along these lines which is at least suggestive. He lays stress in his conception of the 
origin of tumors upon the intimate associations of the cells of the normal body as parts 
of an organism, whose varied capacities are normally held in some fashion under mutual 
restraint in subservience to their common welfare. This uiutual relationship, however, 
once destroyed, for example, by the separation of cells or cell groups from their organic 
associations, they assume less highly differentiated characters, their physiological capac- 
ities are no longer held in leash, and these, if the nutritive and other conditions be 
favorable, may express themselves in exaggerated fashion by excessive growth and 
proliferation. 

Ribbert explains the way in w^hich he conceives that the process of cell disassocia- 
tion and release from restraint may occur. Since he does not admit a primary increase 
in the inherent proliferative capabilities of the cells, he cannot assume, as is commonly 
done, that the process is initiated, in carcinoma for example, by the epithelial cells. 
He assumes that the process may start in the connective tissue, which is liable to in- 
crease in amount in response to a variety of influences, notably those which involve 
trauma, or simple inflammation, or replacement hyperplasia. In the starting of carci 
noma of the stomach or intestine, for example, Ribbert asserts that, in many cases at 
least, the new-formed connective tissue cuts off cells or cell groups from their organic 
connections, and claims that in this way alone we may account for the required release 
from the restraints of the organic association and the exuberant aberrant growth which 
follows. 4 

This view is interesting in connection with the frequent association of carcinoma 
with chronic inflammation, which has been already noted. While obviously vague and 
open to man}^ objections, and apparently applicable to but a small group of tumors, 
and while not yet confirmed by experimental results, this view, nevertheless, perhaps 
indicates the lines along which fruitful research may be expected. 

^ Hansemann, "Die mikroscopische Diagnose d. bosartigen Geschwlilste," Berlin, 
1897. see also resume and h\b\\og!Cdi^\iy 'by Aschoff , Lubarsch and Ostertag's "Ergeb 
nisse," Jahrg. v., 1898, p. 22. 

'AVeigert, "Neue Fragestellungen in path. Anat." Deut med. Wochenschr , 1896, 
p. 635. 

^Ribhert, Deut med. Wochenschr., 1895, Nos. 1, 2, 3, and 4, bibl. ; also ihid., 1896, 
No. 30; also "Das patholog. Wachsthum der Gewebe," Bonn, 1896. 

See for opposing views the monograph hy Lvbarsch, "Zur Lehre v. d, Geschwiilsten 
u. Infectionskrankheiten," Wiesbaden, 1899, p. 306, bibl.; also: Ziegler, Mimch. med. 
Wochen., March 8th, 1898, p. 312. 

See also bibliography of cell regeneration in Fuerst, Ziegler's Beitrage, etc., Bd. 
xxiv., p. 454, 1898, and reference to Aschoff ahove. 
18 



274 TUMORS. 



Classification of Tumors. 

It is not possible to-day to make a satisfactorj^ scientific classification 
of tumors ; but the fact that they are comiDosecl of structures which re- 
semble the various mori)hological tyj^es of tissue found in the normal 
body suggests a grouping of the various forms which may be regarded 
as a useful and suggestive catalogue. 

It should be remembered that the usual separation of the normal tis- 
sues into groui^s is useful, rather because it facilitates their study than 
because it expresses absolute and fundamental distinctions ; and the same 
may be said of all the classifications of tumors. An increase of our 
knowledge concerning their structure and genesis will doubtless lead to 
a more accurate grouping of tumors ; but for the present such an arrange- 
ment as that indicated below will be found of practical a alue for the pur- 
poses of study.' 

CONNECTIVE-TISSUE TYPE. 
Normal Tissue. Tumors. 

Fibrillar connective tissue. Fibroma. 

Mucous tissue. Myxoma. 

EmbiTonal connective tissue. Sarcoma. 

Endothelial cells. Endothelioma. 

Fat tissue. Lipoma. 

Cartilage. Chondroma. 

Bone. Osteoma. 

Neuroglia.^ Glioma. 

MUSCLE-TISSUE TYPE-MYOMATA. 

Normal Tissue. Tumors. 

Smooth muscle tissue. Leiomyoma. 

Striated muscle tissue. Rhabdomyoma. 

' The attempt has often been made to classify tumors with reference to the develop- 
mental history of the tissues represented, and if has been generally believed that cells 
once differentiated in the primary embryonic layers cannot again be merged in type. 
While this principle holds good in general, especially for highly differentiated forms, 
certain recent studies have seemed to indicate that even this distinction may not be 
intlexible. However this may be, it is certain that the cells derived from one embry- 
onic layer may under special conditions come so closely to resemble in morphology those 
of another layer, that a structural differentiation, with our present resources at least, 
is not always possible. While, therefore, this, which is called the Mstogenetic jjrindjjle 
of classifiation, is most suggestive and may be useful in connection with other data in 
the study of tumors, it seems to the writer that it is wiser for the present not to base our 
classification too largely upon embr3^ological data in several particulars still subject to 
controversy. 

Consult in this connection the resume of Marchand on " The Eelationship between 
Pathological Anatomy and Embryolog}^" Verb. d. deutschen path. Gesellschaft, Bd. ii., 
p. 38, 1900. 

See also the admirable address by Minot on " The Embryological Basis of Pathology, " 
Science, March 29th, 1901. In this paper, p. 487, the tissues are classified in accordance 
with their genetic relationships. , 

^ The neuroglia, as well as the tumors derived from it. presents marked peculiari- 
ties in structure. While the neuroglia is closely related in genesis to the nervous sys- 
tem, being of ectodermal origin, its structural and functional alliance with the connec- 
tive tissues of the mesoderm seems to the writers to justify for the present purpose its 
grouping among the latter. 



TUMOES. 275 



NERVE-TISSUE TYPE— NEUROMATA. 

VASCULAR-TISSUE TYPE— ANGIOMATA. 

JS'ormal Jlssxe. Tumors. 

Blood-vessels. Angioma. 

Lymph- vessels. Lymphangioma. 

EPITHELIAL-TISSUE TYPE. 

Normal Tissue. Tumors. 

Glands. Adenoma. 

Various forms of epithelial cells Carcinoma, 

and associated tissues. 



Tumors Formed by Various Combinations of Tissue Types. 

Mixed Tumors. 

lu a considerable proportion of tumors more than one type of tissue 
is present, and it is customary to indicate this by comj^ound names, such 
as osteosarcoma, adeno- carcinoma, etc. Discrimination is necessary in the 
use of such names, however, and one should be clear as to what he 
wishes to express in this way. All tumors have a certain amount of 
fibrous stroma which carries the blood-vessels and forms a sustaining 
framework. In the early stages of tumor growth this matrix may be the 
tissue in which the tumor starts, which is either not increased in amount 
or is hyperplastic. Thus in carcinoma of the stomach, the stroma may 
be fibrous in the mucosa or comx30sed of smooth muscle if the stomach 
wall be involved ; but such growths would not be called either fibro- 
carcinoma or my o -carcinoma. It is only when the new tissue assumes 
the characters of an independent growth that it can be justly indicated 
in the compound name. This may not be easy or always possible to de- 
termine, but the desirability of doing so should be held constantly in 
mind. TJnfortuifately the compound name is by some writers used to 
indicate simply the seat of a tumor growth ; in this sense osteosarcoma 
means simply^ sarcoma of the bone and not an association of osteoma and 
sarcoma. 

It should also be remembered in this connection that a tumor of 
mixed type does not alwaj^s, perhaps not often, start as such, but may 
assume this character by metaplasia within the limits of a tissue group. 
Thus the establishment in fibroma of bone or cartilage growth and the 
assumption by the adenomata of the carcinomatous type are common. 
Furthermore, although these mixed forms of tumors may arise second- 
arily by metaplasia, the more or less distinct forms of tissue maj^ finally 
become so independent of one another that some of the metastases from 
such a mixed tumor may show only one tissue tj^pe. The possibilities 
in tissue metaplasia should be taken into the account before assuming. 



276 TUMORS. 

as is too often done, that the multiplicity of related tissue forms in a 
tumor point toward embryonal origin. 



Complex Congenital Growths — Teratoma. 

These are tumors which frequently contain a great number of differ- 
ent forms of tissue, such as A^arious forms of fibrillar connective tissue, 
cartilage, bone, teeth, hair, skin, muscle, and glands. These are most 
frequently found at the lower end of the spine,' about the head and 
neck, or in the generative organs. Some of them probably arise by an 
inclusion of portions of another foetus, and are thus rather malformations 
than tumors in the limited technical sense. Among these are sometimes 
classed other and simpler congenital malformations, such as dermoid 
cysts, congenital angiomata, and the so-called i)igmented naevi or moles. 

Special Tumor Types. 

There are types of tumors which are not readily brought into the 
usual general classifications, since they are formed of special kinds of 
tissue. These have received distinctive names. Thus there are peculiar 
tumors formed of placental tissue called deciduoma ; of tissue resembling 
the adrenals, hyper -iiephroma, etc. 

Lubarsch's Grouping of Tumors for Practical Purposes. 

Lubarsch has suggested the following grouping of tumors, for practical purposes, 
without special reference eitlier to their histogenetic or histological cliaracters: 

1. Tumors which, although differing from the tissues in which they originate in the 
arrangement of their elements, usually increase in size but slightly or temporarily. In 
this group are the teratoid growths and those originating in embryonic displacements, 
such as congenital nsevi, certain gland-like tumors, mj'oma, fibroma, lipoma, chondroma, 
and osteoma. Such tumors are usually of little practical importance. 

2. Tumors which, although conforming in general to the normal tissue type in 
growth and structure, still reveal a considerable independence of their surroundings; 
such are larger myomata, adenomata, angiomata, lipomata, which may grow slowly 
and with interruptions, and may when growth ceases through degenerative processes or 
necrosis undergo retrogression or even disappear altogether. 

3. Tumors which seem to be largely emancipated from the usual physiological con- 
trol of normal tissues, both in the rapidity and extent of growth and in the fixity of the 
cell type in form and function. In this class are the tumors which are destructive and 
invasive in their growth, especially the sarcomata and carcinomata. 

These three classes may in reality be considered to represent only stages in the 
growth of tumors in general ; since the more destructive forms may in early stages con- 
form to the characters of the other groups, while, on the other hand, tumors of the less 
aggressive types may assume the autonomy and significance of the malignant forms. 
These classes of tumors are not of course distinct, and many intermediate types ma}' 
occur, but this grouping seems to the writer fairly to indicate a real difference in char- 
acter and significance in tumors as a whole which it is of practical advantage to recog- 
nize, and which is often lost sight of in the more technical classifications. 

' For a critical summary, with bibliography, of tumors of the sacral legion, see Bont. 
Centralbl. f. Pathologic, Bd. ix., p. 449, 1898. 



TUMORS. 277 



Cysts. 

These structures, for the sake of convenience, are often classed among 
the tumors, although in general characters, structure, and genesis they 
are usually of entirely different nature. 

They may be divided into two classes : 

I. Cysts which develop from pre-existing cavities. 

II. Cysts which originate independently as the result of j)athological 
changes. 

I. CYSTS WHICH DEVELOP FROM PRE-EXISTING CAVITIES. 

1. Retention Cysts. — These are chiefly formed by the accumulation in 
glands or their excretory ducts of the more or less altered secretion of 
the gland. They usually occur as the result of a hindrance to the nor- 
mal discharge, as from inflammatory contractions, pressure, etc. The 
contents of such cysts are usually mucous, sebaceous, serous, or of a 
mixed character. Their walls are the more or less altered walls of the 
original structure. To this class belong comedones, milium, atheroma, 
chalazion, ranula, the ovula Kabothi, milk cysts, and certain serous cysts 
of the ovaries, Fallopian tubes, gall ducts, and uriniferous tubules. 

2. Transudation Cysts.— These arise usually, though not always, as 
the result of a chronic inflammatory process in lymph spaces or serous 
sacs, and among them are to be classed the so-called ganglia, hydrocele, 
etc. Certain of the so-called hsematoceles, in which blood is extrava- 
sated into closed cavities, form a variety of the cysts of this group. 

II. CYSTS WHICH ORIGINATE INDEPENDENTLY AS THE RESULT 
OF PATHOLOGICAL CHANGES. 

1. Cysts Formed by the Softening and Disintegration of Tissue. — Such 
cysts may at first be small and have very meagre contents and no well- 
defined Avail. A^wall may finally be present either as an entirely new- 
formed structure, or the more or less modified caj)sule of the organ in 
which they occur maj^ partly or entirely form the wall. The contents of 
such cysts are usually the more or less altered detritus of the tissue by 
whose disintegration they are formed. Such cysts are very apt to occur 
within true tumors, particularly those which are succulent and of rapid 
growth, since these, as above stated, are very liable to degeneration. Old 
abscesses may change into well-defined cysts of this kind. 

2. Cysts Formed around Foreign Bodies. — The inflammatory reaction in- 
duced by the i^resence of foreign bodies of various kinds, parasites, 
masses of extravasated blood, etc. , frequently results in the formation of 
well-defined encapsulated cysts. 

3. Cysts Formed by a New Growth of Tissues in whose Spaces Various 
Kinds of Fluid Accumulate. — These spaces may or may not be lined with 
epithelium and have something of the glandular character. Such forms 



278 TUMORS. 

are exemplified in some of the compound ovarian cysts — the so-called 
ovarian cystomata ; but these are I'eally adenomata. 

4. Congenital Cysts. — These are of various forms, and their mode of 
origin is in most cases but imperfectly understood. Some of them are 
properly grouped among the teratomata. The so-called dermoid cysts of 
the subcutaneous tissue (Fig. 135) and ovary are marked examples of 
this class. Certain congenital cysts of the kidney and other internal 



;,.;i^'^f'=f|gi^f^|^^ 






< ,-;-" '4". -> '.^ '--^ ^^" A.. /•• 






'^V ..;^>, 













Fig. 135.— Dermoid Cyst of the Skin. 

This small cyst beneath the skin above the eyebrow is lined with epithelial cells, in places cuboidal in 
form but mostly merged Into an irregular cell mass. The flbrous-walled cyst contained a clear fluid and a 
little frranular cell detritus. 

organs are conveniently grouped here, although it is quite probable that 
some of them at least originate during foetal life in one or other of the 
above -described ways, and hence are not essentially different in nature 
from some of the cysts of other classes. For the mode of formation of 
certain cysts of the neck see page 486. ' 

Various Lesions Sometimes Described as Tumors. 

There are certain enlargements of the lympli-nodes which are in reality hyper- 
plasias, sometimes inflammatory in character and sometimes not, and which are often 
grouped among the tumors as lympJiomata. They are not true tumors, and will be con- 
sidered under the lesions of the lymph-nodes. In the same group are often classed the 
enlargements of the lymph-nodes in leukaemia and in other general diseases, which are 
considered in another part of this book. 

Another group of tumors sometimes called lymphomata are in reality sarcomata, 
and these will be described under the latter heading. 

There is also a group of nodular new formations, the so-called infective granulomata, 
which in earlier days were classed among the tumors. These are found in tuberculosis, 
lupus, leprosy, syphilis, glanders, and actinomycosis. They are, however, inflamma- 
tory new formations, and, as our knoMiedge regarding them has increased, many of 
them have been proven to be incited by plant parasites (see section devoted to Infectious 
Diseases). In the case of syphilis the absolute proof is still lacking. 

' Consult for consideration of ciliated and other cysts, Hess. Ziegler's Beitr. zur path. 
Anat., Bd. viii., p. 98, 1890; also Zahn, Virchow's Archiv, Bd. cxliii., p. 170, 1896. For 
later general bibliographv of cysts see Aschoff. Lubarsch and Ostertag's " Ergebnisse, " 
Jalirg. ii. for 1895, p. 456." 



TUMORS. 279 



Technique of Fixation and Hardening.^ 

In genei'al, tumors, like all tissues for microscopical study, should be cut into small 
pieces before immersing them in the preservative tluids. and the sooner they can be 
placed in these after removal the better will be the preservation. In some cases much 
may be learned from large sections of tumors together with their surrounding tissues. 
In this case the suitable portion of the tumor must be preserved whole, and is best har- 
dened in strong alcohol. 

It is often important in the study of tumors to examine not only the fully devel- 
oped or mature tumor structures, but also those portions in which the new growth is 
forming and in which it is encroaching on adjacent parts. 

So that in selecting portions of tumors for preservation and study, it is not wise to 
snip off a small piece at random, but a careful selection should be made, liberal por- 
tions being saved, from the centre, from the periphery, and from such surrounding 
tissues as are available. For the ordinary routine hardening of tumors, Orth's fluid 
followed by alcohol may be recommended. 



Special Forms of Tumors. 

FIBROMA. 

The fibromata are composed of fibrillar connective tissue, which, as 
in the physiological type, is sometimes dense and firm. Fibroma durum, 
and sometimes loose in textnre and soft. Fibroma molle. They are usu- 
ally sharply circumscribed and are frequently encapsulated, but they 
may be diffuse and merge imperceptibly into the surrounding tissue. 
They are frequently small and insignificant, but occasionally grow to an 
enormous size. Some fibromata consist almost entirely of intercellular 
substance, containing but few flattened or spindle-shaped cells (Fig. 136) ; 
others contain very many variously shaped cells (Fig. 137). The cells 
are often more abundant in one part of the tumor than in another. The 
denser A^arieties usually contain but few blood- 
vessels, although they are occasionally quite ^ " ' -. ' 
vascular. Many of the softer varieties are . \ ' ^ , -- -^ 
very vascular. Xerves are occasionally pres- 
ent. The course and arrangement of the ' , '% 
fibres in these tumors are usually irregular, . . ^ 3 
often crossing and interlacins: in a most com- " ' \ ' ', C^^' 
plex manner. The fibromata are usualh^ of ^ , ' ^, ' 'J^ 
slow growth, but exceptionally they giow , , ^ ' 
rapidlv. Thev are benign tumors, but by 

^ - - * 'J Pj^^ 13b.-Dr.N-r. FibRv--<r.A OP 

pressure on miportant organs, by ulceration, abdomixal wall- fibroma 

or by changing into other varieties of tissue, i^^Ri'^f- 

thev may become of serious import. Pure some of the bands of connective- 

•^ tissue fibres are cut across, otbers 

fibromata do not form metastases, but thev are cut lengthwise. 



are often multiple, and when so are fre- 
quently congenital. They may recur when not fnlly removed. 

It seems probable that in the multiple fibromata of the skin {Fihvoma 
moUuscum) the new growths occur in some special form of connective 



280 TUMORS. 

tissue, as that of the nerves, blood-vessels, or glands. Some of them are 
congenital. There is often a growth of very cellular tissue just beneath 
the epithelium. Such tumors resemble sarcoma. ' 

While the fibromata are commonly nodular in form, when they de- 
velop on the skin or mucous membranes they frequently form papillary 
outgrowths covered more or less thickly with epithelium, and are then 
cslled jxqjiUomata (Fig. 138). Common warts of the skin are papillomata 
with excessive production of surface epithelium. To the papillomata 
also belong some of the so-called condylomata. 

The so-called Cheloid, composed of very dense fibrous tissue with few 
cells, often de^'elox)S rapidly in old cicatrices, or elsewhere, in the skin, 




Fig. 137.— Fibroma Molle ; from the Subcutaneous Tissue. 
The stroma is oedematous, and in gross appearance the tumor resembled myxoma. 

forming flat or slightly lobulated tumors. It is not in all cases clear 
whether cheloids should be regarded as tumors or as inflammatory new 
formations. 

Fibromata are frequently combined with other kinds of tissue to form 
complex tumors. The looser, softer varieties not infrequently become 
oedematous, when they may closely resemble myxomata (Fig. 137). 
Fibromata are liable to calcification and to fatty and mucous degenera- 
tion. By metaplasia they may partially change to form fibro- chondroma, 
fibro -lipoma, fibro- sarcoma, or fibro-osteoma. The latter transformation 
frequently occurs when they form in the periosteum. 

Developing, as they do, in the connective tissue, fibromata occur in 
the various parts of the body : in the skin and subcutaneous tissue ; in 
intermuscular tissue and f ascise ; in periosteum ; in the nerve sheaths and 
intrafascicular connective tissue ; in the dura mater, the interstitial tissue 
of organs, and in the mucous membranes. Some of the so-called polypi 

^See GilcTirist, Johns Hopkins Hospital Reports, vol. i.. p. 349, 1896. 



TUMORS. 



281 



of the mucous inembraues (see Fig. 139) and some psammomata are forms 
of fibroma, the former often approaching the myxoiiata in structure. 







Fig. 138.— Small Papilloma of the Skin. 



Occasionally, in the ducts of glands, fibrous polypi grow to an enor- 
mous extent, their epithelial covering keeping pace in growth with their 




l? ^^^^ "^ 







T. - 



^- 















Fig. 139.— Mucous Polyp of the Nose. 

The section shows the epithelial covering of the new growth, as well as its numerous blood-vessels and a 

few mucous glands. 



282 TUMORS. 

de\ elopmeut, until they form very large, irregular, loose-textured tumors, 
which often finally ulcerate. Such forms are seen in the mammary 
gland, where they are sometimes mistaken for carcinomata. They are 
called Intracanalicular Fibromata (see Fig. 383, page 643). 

It is often difficult to distinguish between genuine fibromata and in- 
flammatory or other connective -tissue hyperplasias, such as elephantiasis ; 
and perhaps the fuller knowledge of the future will show that the dis- 
tinctions are not as definite as our classifications indicate. 



MYXOMA. 

Mucous tissue is essentially an embryonic tissue, for in the normal 
adult it is present only in a very imperfect and atypical form in the 



% ( 



V. 



I '' ■'/ '- / \ 



-_ _ - . ( \ ■ ' ^ 



-A 



fj -., ^: ^- 









Fig. 140.— Myxoma of the Larynx. 
Showing the diffuse staining of the mucin-containing stroma with haematoxylln. 

vitreous of the eye, and perhaps exceptionally in small amount about 
the heart, kidneys, and medulla of bone. 

The myxomata are thus essentiallj^ embryonic-tissue tumors. These 
tumors consist, in their most typical forms, of a homogeneous or finely 
fibrillated, soft, gelatinous basement substance, in which are embedded a 
variable number of spheroidal, fusiform, branching, and often anas- 
tomosing cells (Fig. 140). They may contain few or many blood-vessels 
and sometimes nerves. By the addition of acetic acid, mucin may be 
precipitated from the basement substance. In sections it is usually 
stained with hsematoxylin. The very soft forms which contain compara- 
tively few cells and much translucent basement substance are called 
Myxoma gelatinosum or M. molle. The presence of many cells renders 
them more consistent and gives them a whiter and more opaque appear- 
ance ; such forms are called M. medullar e. 

Pure myxomata are not common. The myxomata are very apt to be 
combined with fibrillar connective tissue as fibro-myxoma ; or with fat 



TUMORS. 283 

tissue, lipo-myxoma ; and they ^'ery frequently become sarcomatous, or 
take part in the formation of very comj^lex tumors. They may be dif- 
fuse or encapsulated with fibrillar connective tissue ; they are frequently 
very large, and may be multiple. Owing to the character of the base- 
ment substance, the blood-vessels not infrequently rupture, giving rise 
to larger or smaller haemorrhages within the tumor, or to the formation 
of cysts. The cells are liable to undergo fatty degeneration. 

In the fibrous tissue of many tumors, in chronic intiammation of the mucous mem- 
branes, variously shaped small cells occur whose bodies contain few or many well- 
defined basophlle granules which are not infrequently mistaken for cocci. Such cells, 
called "mast cells," occur in various parts of the normal ho&y. The nature of the 
granules has not been definitely determined. 

Composed, as tliey are, of a type of tissue from which fat tissue is 
developed in the embryo, the relations of myxomata to fat tissue are 
very intimate. They are most frequently developed in, and probably 
directly from, fat tissue. Thej^ are also found in the subcutaneous, sub- 
mucous, and subserous tissue, in the marrow and periosteum ; in the 
brain and cord ; in the sheaths and intrafascicular tissue of peripheral 
nerves; in intermuscular septa ; and in the interstitial tissue of glands, 
such as the mamma and parotid. 

The myxomata are in general benign ; yet they are very prone, esi^e- 
cially the lii)omatous forms, to local recurrence. They sometimes grow 
very rapidly, and sometimes, though very rarely, form metastases. In 
the not infrequent combination with sarcoma they may exhibit the most 
marked malignancy. Some of the polyi3i of mucous membranes are 
apparently myxomata or fibro-myxomata. On the other hand, many of 
the so-called mucous polyi^s, those of the nose for example, are simply 
oedematous hyperplasise of the mucosa. ' 

O^dematous, loose, and cellular forms of fibrillar connective tissue 
so closely resemble some of the forms of mucous tissue that certain 
observers consider them identical. So prone are many tumors to un- 
dergo mucous degeneration, and so frequent are the combinations of the 
myxomata with i)ther forms of tumors, that it is often difficult, some- 
times impossible, to say whether the mucous tissue in a given composite 
tumor is primarj^ or secondary. 



SARCOMA. 

These tumors are formed on the type of connective tissue, but they 
are, as a rule, largely composed of cells ; the basement substance, though 
a constant and important factor, being much less consi)icuous than in 
adult connective tissue. They more closely resemble, in general, the 
developing connective tissue of the embryo or the granulation tissue of 
inflammation. 

The cells of the sarcomata are most varied in size and shape. The^^ 

^ See reference to Wright, p. 429. 



284 TUMORS. 

may be flat, fusiform, spheroidal, or branched, and even cuboidal or 
cylindrical ; they may be mnltinnclear and very large, or they nvdj be 
very small and spheroidal, resembling leucocytes. The fibrillar base- 
ment substance may be ]3 resent in such small cxuantity as entii-ely to es- 
cape a superficial observation, covered as it may be by the abundant 
cells; or it may be so abundant as to give the tumor the general appear- 
ance of a fibroma. It may be intimately intermingled with the cells in 
fascicles, or it may be in large open -meshed networks, giving to the 
tumor an alveolar appearance. The cells, however, always stand in an 
intimate relationship to the basement substance, which they sometimes 
reveal by fibrillar processes continuous with it. Blood-vessels also form 
a constant and important structural element in these tumors, being in 
some of them so predominating a factor that they give structural outline 
and general character to the growth. They, too, as in the normal con- 
nective tissue, are intimately associated with the basement substance and 
with the tumor cells. 

Sarcomata are most frequently found in the skin, subcutaneous tis- 
sue, fasciae, subserous connective tissue, the marrow or periosteum, and 
in the choroid. They may also occur, though more rarely, in the dura 
mater; brain and cord; lymph-nodes; in the adventitia of blood-vessels, 
and in nerve sheaths ; in submucous tissue ; in the uterus and ovary, 
and in the kidney. In the liver and lungs and heart they may occur by 
metastasis. 

They are most common early in life. The cellular character, the 
rai)id growth, the vascularity and succulence of many forms, the marked 
tendency to local recurrence, and the formation of metastases, stamp the 
sarcomata as malignant tumors. But in this they vary greatly ; while 
some of the forms belong in every sense to the most malignant of tumors, 
others grow slowly, are very dense, and may remain localized and harm- 
less for years. Their tendencies in this respect will be mentioned under 
the special forms. 

Intimately related as they are to the blood-vessels, metastasis is more 
apt to occur through the blood than through the lymph channels, and 
consequently adjacent lymph-nodes are much less apt to be involved than 
in some other forms of tumor, notably the carcinomata. The richly cel- 
lular and vascular forms of sarcoma are especially prone to hsemorrhages, 
degeneration, and ulceration. 

A single form of cells is often so predominant as to furnish a suitable 
qualifying name for the tumor, but in many cases the cell form varies 
greatly in the same growth. It may be said, in general, that there is a 
tendency to reproduce in these tumors some of the special characteristics 
of the tissues in which they originate. Thus, sarcomata of the bones are 
apt to be osteo -sarcomata ; those of pigmented tissue, like the choroid, 
are apt to be pigmented sarcomata. It will be more convenient for our 
present purpose to describe briefly the more common forms one after 
another than to attempt any systematic classification of them. It should 
be remembered, however, that the various forms are not sharply defined, 



TUMORS. 



285 



but are apt to merge into one another and to intermingle in various 
ways. 

Spindle-celled Sarcoma. — The cells in these tumors may be large — large 
spindle-ceUed 8. (Fig. 141) ; or they may be small — small spindle -celled 8. 







^ $0 cs\\ 



'*'} ^'J- rsi 




Fig. 141.— Large Spindle-Celled Sarcoma. 



(Fig. 142). They may consist largely of cells, or may contain so much 
intercellular fibrous tissue as to be appropriately called fibrosarcoma. 
The cells are frequently arranged in fascicles, which surround the blood- 
A^essels, and these fascicles may cross and interlace. These tumors, espe- 
cially the small -celled forms, are, as a rule, denser and firmer and less 
malignant than other forms of sarcoma, but to this there are many ex- 
ceptions. They may be encapsulated or infiltrating. To this class be- 
long the growths formerly described as fibro-plastic tumors and recurrent 
fibroids. They frequently occur 
in the periosteum, subcutaneous 
tissue, and muscle ; in the uterus, 
and in various glands, notably in 
the mamma, testicle, thyroid, etc. 
These forms are among the most 
frequent of the sarcomata. 

Round-celled Sarcoma. — Of 
these there are two classes — 1, 
small round-celled sarcomata and, 
2, lay^ge round-celled sarcomata. 

1. The small round -celled sar- 
comata consist of cells of about 

the size and appearance of mononuclear leucocytes (Fig. 143), and may 
have much or little intercellular substance, which may be irregularly dis- 




FIG. 143.— SMALL 



Spindle-Celled 
Forearm. 



Sarcoma of 



.S^ ' '^^ '^ir^'^g^ They most frequently occur in the 

^^ ^V(.^y X^^^V^^"" \^ ^^^ ^^f<^ connective tissue of the muscles and 



286 TUMORS. 

posed 01^ arranged in large meshes resembling alveoli. In many cases, 
so small is the quantity of intercellular substances that it is difficult of 
detection without special modes of preparation. These tumors often 

contain many blood-vessels, and may 

^ ^ r^ (?) <r^ , ^ »r be verv soft and succulent. Their 

®roV^^^^^ <%''^^ ' j^rs^^^^ ' oTOwth is sometimes rapid and thev 

^^ ^ ,^ , ^ v^r ^ ^ are often very malisrnant. 

fc ^ o^V^^^'.?*-^ '^^^'x*^ ^^ (?7/w?^/?o-s«reom«.). They also occur 

^ ^^?^ft ; ^^ ^ c; ^ 2^y/'< %? ^ ^ in the internal organs, not infrequently 

f^^^®^^^> f \ %\ io^ t^ iii the brain, associated with glioma 

as gJio-sarcoma. 

Fig. 143.— Small Round-Celled Sarcoma. 2. Ill the large rOUlld-celled Sarco- 

From a metastatic tumor in the lungs. mata (Fig. 14:4:) the CCllS A^aiy ill sizC, 

but are usually very much larger thau 
in the last variety. Their nuclei are usually large and contain prom- 
inent nucleoli. They, too, are often very vascular, and contain a vari- 
able quantitj^ of basement substance. They are occasionally alveolar 
in character. They are, as a rule, less soft and malignant than the 
small -eel led varieties. 

Melano-Sarcoma. — These tumors consist most frequently of polyhedral 
cells of various sizes. They are characterized by the presence in the 
cells, and less frequently in the intercellular substance, of larger and 
smaller particles of brown or black pigment (Fig. 145). The pigment 
is usually ([iiite irregularly distributed in patches or streaks. They arise 
most frequently in the skin and in the choroid. Pigmented moles of 
the skin often form their start- 
ing-points. They belong to the ,. _^ ^1^ 
most malignant of tumors. They ^^i ,.,, ;, '^' 
very readily form metastatic tu- , ^'1 ^ 
mors in various parts of the ^ ' ^> 

body, which are, like the parent .v' '\. i^ {. r^ ' 

* . , - " "'-''' J, ^ 

tumor, pigmented. T'"'' ''' ^^ 

Various forms of tumors may ^\ ' "-'" ,/-> ^ 6 

contain brownish pigment de- 
posited in them by the degenera- 
tion of the hsemoglobin from ex- 
travasated blood; these should 
not be mistaken for melanotic 
sarcomata. ' 

Myeloid or Giant-celled Sarcoma. — Tumors of this class are usually 
formed chiefly of spheroidal or fusiform cells of variable size, but their 
characteristic feature is the presence of larger and smaller multinuclear 

' On the occurrence of melanuria in cases of melano-sarcoma consult Timelier , Trans- 
actions New York Pathological Society, 1893, p. 105. 



i^' 



Fig. 144.— Large Round-Celled Sarcoma. 

A tumor of the mamma. Mitotic figures in some of 
the cells. 



TUMORS. 



287 



cells, called giant cells. These are closely intermingled with the other 
cells, and may be very abnndant or very few in nnmber (Fig. 146). 




Fig. U5.~Mklaxo-Sarcoma. 
Tumor from submaxillary region. 

Giant cells may occasionally occur in other tumors, but are most abun- 
dant and characteristic in these. These tumors are chiefly formed in con- 
nection with bone, and may originate in the marrow or in the perios- 
teum. They are sometimes very soft and vascular, and subject to 
interstitial haemorrhages. Some of these vascular sarcomata were formerly 




Fig. 146.— Giant-Celled Sarcoma of Bone. 



classed together with other kinds of vascular tumors as fungus h?ema- 
todes. Some of the forms of epulis are giant -celled sarcomata. 

When these tumors originate in the marrow of the long bones, which 
is a favorite place for them, they are apt to cause resorption of the bone ; 



288 



TUMORS. 



and although the tumor may be for a long time enclosed by a shell of 
new-formed bone, which enlarges with the enlarging tumor, it usually, 
sooner or later, breaks through this and infiltrates adjacent tissues. 




Fig. 147.— Angio-Sarcoma of Liver. 
The thin-walled blood-vessels, around which the tumor cells are formed, are irregularly dilated. 

They are liable to form metastases and frequently grow to a very great 
size. The periosteal forms are apt to be firmer in texture, and are prone 
to the development of irregular masses of new bone within them, thus 
forming one of the varieties of osteo- sarcoma. 

Osteo-Sarcoma, — These are spindle or round-celled tumors, usually, 
but not always, connected with bone, in which irregular masses of bone 






'"~^'^\ y-^' 

- " ^-^i-; 



D 



Fig. 148.— Angio-Sarcoma. 
Tumor from the arm. Sometimes called perithelial sarcoma. 

tissue are present. The bone is usually of irregular atypical structure, 
the regular lamellation and typical Haversian canals being usually ab- 
sent. They may form metastases which present similar characters. 



Fig. 149.— angio-Sarcoma. 



TUMORS. 289 

Angio-Sarcoma. — lu many of the sarcomata in various parts of the 
body the blood-vessels form so promiuent and Important a feature as to 
give special character to the growth, not alone by their size and general 
prominence (Fig. 147), but sometimes by the peculiar arrangement which 

their presence gives to the cells. 

..^'^ t'^i^r^^^-. While in most of the sarcomata 

'-. . the blood-vessels have a very im- 

^ t \ portant influence in determining 

i^ ^-_ -^^ '\, the topography of the tumor, in 

^■^^ ^ ^ --. most of the denser and in many 

, .^^ ; . of the softer varieties this influ- 

^>-"'~3^'-:-"'^ ence is not easily traced. In 

, ,-, many forms, however, particu- 

. . 5 - . ^ y/.^^ ^ larly those which are soft and 

^^ ViJ,' . "^ very cellular, the cells are closely 

grouped around the vessels, de- 
veloping in their adventitise and 

One of the blood-vessels with Its cellular sheath from „ . i ^ i n < i 

the tumor shown in Fig. 148. forming shcaths arouud them 

(Fig. 148 and Fig. 119). The 
masses of cells thus formed, with a blood-vessel for a centre, may be 
closely packed together in long strings with more or less frequent anas- 
tomoses or they may be arranged in rounded groups, giving to the tumor 
an alveolar ax)pearance (Fig. 150). Such tumors are called angio-sarco- 
mata. Simple vascularity, although this be extreme, does not make 
of a tumor an angio-sarcoma. 

Alveolar Sarcoma. — Sometimes, as above stated, the basement sub- 
stance of the sarcomata, particularly in some of the round-celled varie- 
ties, is quite abundant and arranged in a wide -meshed net, in the meshes 
of Avhich the cells lie. These 

spaces are called alveoli, and j ^" ^- ^^ 

this variety of structure has ' "^ ^^^/ , % ' - '^' ^^^ "^ ^ ^ ' ' \ 

acquired importance from the z'*' ' ^ ^ ^ ^ . l^^ '^'1 

general resemblance which f ' '' '- ^ 

these tumors have to the well- .-. ^ 1? ^ - <^ - 

defined and characteristic alve- \ ^ .. T^^'^® -*/'' "^^^ J 

olar structure which manv of ^ ^^ f^^"^ ^^ ,^ ' "^ 

the carcinomata exhibit. It ' ^. ^ " ,^ 

is true that occasionally the 4 - n ^ ^ ' -■ ^> -" ^^--^^ \ 

resemblance is very close in- ^"'^ 

deed, but usually the sarcomata fig. 150.- angio-sarcoma. endothelioma ? 

present a more or less intimate Tumor of lymph-node. 

relation between the cells and 

basement substance. The cells usually do not simply lie in the cavities, 
but are often attached to the intercellular substance, which not seldom 
sends finer trabecule into the alveoli between the cells. Sometimes a 
careful shaking of sections in water is necessary to reveal the characters 
of the reticulum. The cells, moreover, are usually, though not alwavs, 
19 



290 



TUMORS. 



distinctive in character. This form of tumor is, in some cases at least, 
determined, as above stated, by the new formation and peculiar arrange- 
ment of the blood-vessels. Tumors of this kind are not common, but 




Fig. 151.— Myxo-Sarcoma of Pharynx. 



may occur in the skin, lymph- nodes, bones, and pia mater. They are 
usually very malignant. Many of these tumors are doubtless more 
properly classed among the endotheliomata. 

Mixed Forms of Sarcoma.— In addition to the above more or less well- 
defiued forms of sarcoma, there exist various modifications which have 
received special names. The sarcomata in which cysts form, either by 
the softening of tissue by degeneration, or by the dilatation of gland 



,M'ki 














Fig. 153.— Adeno-Sarcoma of Parotid. 



ducts by pressure, or by the new formation of tissue in gland ducts or 
alveoli which dilate with the growth of the tumor, have received the 
name of cysto- sarcomata. 

Mucous degeneration is frequent in the various forms of sarcoma. A 



TUMOES. 291 

combination of myxoma and sarcoma — myxosarcoma — is common (see 
Fig. 151). 

Combinations of sarcoma with fat tissue, lipo-sarcoma ; \rith glandu- 
lar structures, adeno- sarcoma (Fig. 152) ; with cartilage, chondrosarcoma ; 
with muscle tissue, myosarcoma ; and with various other tissues, are of 
frequent occurrence. Some forms of psammoma, or ^^ brain sand,^' found 
chiefly in the dura mater, Sjre Jib ro sarcomata which have undergone cal 
cification, the lime being deposited in lamellated masses of various shapes 
within them. 

Some of the soft papillomata and warts, and occasionally the polypi 
of the mucous membranes, belong to the type of sarcoma or myxo- 
sarcoma. 

The so-called chloromata, which have been found in a variety of places 
in the body, but are rare, are apparently forms of sarcoma. Chloroma 
is characterized by a greenish color, the nature of which is not known. ' 

ENDOTHELIOMA. (Endothelial Sarcoma.) 

Under the name endothelial sarcomata or endotheliomata are grouped a 
number of tumors which on the one hand are closely related to the sar- 








^iT ^^«,/ — ^N 










Fig. 153.— Endothelioma of Upper Jaw. 
Showing dense connective tissue surrounding the blood-vessels between the reticular endothelial cell 



comata in genesis, and in some cases in appearance, while on the other 
hand some of them so closely resemble some forms of carcinoma as to be 

1 For the relationship of chloroma to leukaemia see Book, American Journal of the 
Medical Sciences, August, 1893, bibliography. 



292 



TUMOES. 



with difficulty distinguished from them. The endotheliomata originate 
in that form of connective -tissue cells called endothelium, lining blood 
and lymph vessels or lymph spaces, and develop by a proliferation of 




Fig. 154.— Endothelioma of Antrum. 
This complex form of endothelioma, resembling types of adenoma, not infrequently occurs in the ovary. 



«^-^?> 









these cells (Fig. 153). Sometimes the cells of the endotheliomata re- 
semble closely the normal endothelium ; sometimes, however, they differ 
considerably from them, being occasionally very large, often thick and 
irregular in shape, and even nearly cylindrical or cuboidal like certain 
forms of epithelium (Fig. 154). They are associated with a more or less 

abundant vascular stroma, 
which may be alveolar in 
formation. In this case, as 
in alveolar sarcoma, it may 
often be seen that the cells 
have an intimate relationship 
to the trabeculse of the stroma. 
Developing from the en- 
dothelium of the vessels or 
lymph spaces, these tumors 
sometimes exhibit a structure 
closely simulating that of 
tubular glands lined with 
more or less cuboidal epithe- 
lium or papillary angio- sar- 
comata (Fig. 155). It is in many cases difficult to decide from the 
structure in the fully developed parts of a tumor whether it is an en- 
dothelioma, an adenoma, or a carcinoma. In such cases a careful study of 







- xm 



Fig. 155.— Endothelioma of Humerus. 
Type resembling angio-sarcoma. 



TUMOES. 



293 



the peripheral portions of the tumor and parts into which it is extending 
may reveal early phases of proliferation in the endothelium of lymph 






'JrC 




FIG. 156.— Endothelioma (Endothelial Sarcoma) of Dura Mater. 



'^ ,\ 






::>, — 7 •J* 



^ ci. '^- 



^€ . ..^-^^'^-: ^cr 









-'OO y '-^ (£, 


»*- -v* -, _ _ 




..o _ , ^ 


--, t ",S 


,rDr^ ^ . -. ^ 


V-Id> " 


* . '^ - T 












: -^no^-- 


oo oo^ 














^s» 




^^ CO 







^ -5^ 






^^(^^''v^'' ^? 






^ 



Fig. 157.— Endothelioma of Pleura. 
Showing the formation of mucus within the endothelial cell masses ; the mucus is stained with hematoxylin. 



294 TUMORS. 

vessels or spaces. In this case its genetic relationship may throw light 
on the nature of the tumor, however similar it may be in morphology to 
carcinoma. 

Sometimes the cells of the endotheliomata are packed together in 
dense concentric masses (Fig. 156), which may have a glistening appear- 
ance, and such tumors are sometimes called cholesteatomata. Although, 
for the most part, the peculiar glistening appearance of these tumors is 
due to the closely packed thin cells which compose them, they not infre- 
quently contain crystals of cholesterin, which may share in producing 







Fig. 158.— Endothelioma of Upper Jaw, 

Showing formation of mucus in the gland-like endothelial cell masses. This form of tumor is often called 

"cylindroma." 

this characteristic appearance. But the cholesterin may be absent, or 
present in small amount. 

The stroma of the endotheliomata may undergo various forms of 
alteration, developing hyalin, myxomatous, or cartilaginous or very 
dense fibrous characters (Fig. 153) ; or it may atrophy, leaving the pro- 
liferated endothelium and the blood-vessels as the chief structural ele- 
ments. On the other hand, hyalin and mucous degeneration of the endo- 
thelial cells may occur (Fig. 157), and considerable collections of these 
materials, free from the cells but surrounded by the cell masses, may 
give a cystic character or lend a glandular appearance to the growth. 

Such tumors— in which homogeneous or striated cylinders of hyalin 
or mucoid material (Fig. 158), often closely surrounded by layers of 
cuboidal or flattened cells (Fig. 154), form a striking feature — have 
sometimes been called cylindromata. The stroma of the endothelioma 



TUMORS. 295 

may become sarcomatous and thus a mixed tumor — a sarcomatous endo- 
thelioma — may be formed. 

The endotheliomata may be single, nodular, and of considerable size ; 
or they may be multiple, numerous small tumors being scattered over 
the surface of the part in which they grow. They may even form a 
thick or thin pellicle over surfaces, or cause adhesions between adjacent 
organs. They may form metastases. They occur in the dura mater and 
pia mater, in the pleura and peritoneum, and have been described in the 
skin, bone, gums, lymph-nodes, ovary, liver, brain, testicle, glandula 
carotica, and salivary glands. ' 

It is possible that as our knowledge of these tumors widens we may 
be able to differentiate a group formed from the cells lining the great 
body cavities — peritoneum, pleura, and pericardium — which are usually 
called endothelium, but might, as is urged by Minot, on account of their 
origin and in distinction from the endothelium of the blood and lymph 
vessels, etc., be more appropriately designated mesothelium. '^ 

LIPOMA. 

Lipomata are tumors formed of fat tissue. The fat tissue occurs in 
lobules and is similar to normal fat, except that the cells and lobules are 
usually larger and less regularly arranged. There may be little connec- 
tive tissue in the tumors, when they are very soft, almost fluctuating — 
lipoma molle — or there may be so much as to give the tumor considerable 
firmness^?&ro-7?j:>owi«. They may be in part transformed into mucous 
tissue — my xo -lipoma. Cartilage not infrequently develops in them, or 
they may undergo partial calcification. 

Occasionally the blood-vessels are very abundant and dilated — angio- 
lipoma. They are usually sharply circumscribed, but may infiltrate sur- 
rounding tissues. They are not infrequently pediculated. They some- 
times grow to enormous size and may ulcerate. 

They are usually isolated, but may be multiple. They are common 
tumors, occurring usually in the subcutaneous or other fat tissue. They 
may occur in the mucous membrane of the gastro- intestinal canal, in the 
peritoneum, more rarely in the dura mater, kidney, liver, and lungs. 
They are benign tumors, not forming metastases ; but they may be dele- 
terious by ulceration or gangrene, and when not fully removed may ex- 
hibit local recurrence. They may become sarcomatous. 

^ For a discussion of the endotheliomata consult : 

i\ Volkmann, "Ueber endotheliale Geschwiilste." Deutsch. Zeits. f. CInrurgie, Bd. 
xli., p. 1. 

Lubarsch, "Ergebnisse d. allg. Path.," Jahrg. i., Abth. 2, p. 366; also "Endothe- 
liom.," ibid., .Jahrg. ii., p. 592. 

For embryological considerations bearing on the subject see: 

Glockner, Zeits. f. Heilkunde, Bd. xviii., p. 209, 1897. 

Marchand, Verb, der deutschen path. Gesellschaft, Bd. ii., p. 38, 1900. 

On the occurrence of s^iant cells and cells with very large nuclei in endothelioma, see 
Glockner, Ziegler's Beitr.,''Bd. xxvi., p. 73, 1900. 

- For a consideration of the relationship between endothelium and mesothelium see 
Minot, Science, March 29th, 1901, p. 489. 



296 TUMORS. 



CHONDROMA. 

These tumors, composed of either of the forms of cartilage, are usually 
hard, but sometimes quite soft. The cells do uot present the same uni- 
formity in size, shape, number, and relative position that they do in nor- 
mal cartilage (Fig. 159). Sometimes they are very large, spheroidal, and 
grouped in masses, and again small and far apart. Thej" are frequently 
fusiform or branching. Fibrillar connective tissue in varying quantity 



Fig. 159.— Chondroma of Femur. 

is usually present in the chondromata, either as a capsule or running in 
bands between the nodules of cartilage, or passing in fascicles into them. 
The cartilage may change to mucous tissue, forming myxochondroma, 
the cells may undergo fatty degeneration or they may calcify or ossify. 
Chondromata frequently form a part of mixed and complex tumors. 
Metaplasia plays an important part in the development of cartilage 
tumors of mixed type. 

They may form in connection with bone or cartilage, and are often 
traceable to irregularities in foetal development. Or they may occur in 
soft parts where cartilage is not normally present, as in the parotid, tes- 
ticle, mamma, and ovaries, where they are a]3t to be mixed with other 
tissue ; or in subcutaneous connective tissue and fasciae. 

They are in general benign tumors, but metastases sometimes occur, ' 
most frequently in the lungs, sometimes in the heart. 

Small hyperplastic growths on the surfaces of cartilages are called 
ecchondroses. 

OSTEOMA. 

The formation of bone in the body in abnormal places occurs quite 
frequently and under a great variety of conditions. It is on this account 
not easy to define the term osteoma, and it is frequently difficult to de- 
cide whether or not a given mass of new-formed bone should be thus 

' For a study of metastases in chondroma see Ernst, Ziegler's Beitr., Bd. xxviii., p. 
255, 1900, bibl. 



TUMORS. 



297 



designated. Bone tissue often occurs in tumors of the connective-tissue 
group as a secondary or complicating structure — osteo-fibroma^ osteo-clion- 
dromcij osteosarcoma, etc. It may occur in muscles as a result of certain 
exercises, or as a result of a peculiar inflammatory process, or it may 
occur in connection with chronic inflammation in a variety of tissues. A 
circumscribed mass of abnormal bone, not of inflammatory origin, may 
be called an osteoma. Small masses of new-formed bone of various 
shape, projecting from a bony surface and frequently of inflammatory 
origin, are usually called osteophytes. Bony tumors projecting from the 
surface of bones are frequently called exostoses. 

An osteoma may be loose in texture, consisting of bone tissue similar 
to cancellous tissue ; or it may be very hard and dense like ivory, so- 
called ivo}^y exostoses. The difference between these forms lies chiefly 
in the varying number and size of the vascular and medullary spaces 
which they contain. The growth of the osteomata is, as a rule, slow. 
They are benign tumors, and are not infrequently multiple. 

Osteomata may develop in connection with the bone or periosteum, 
which is most frequently the case, or, independently of bone, in soft 
parts. 

New-formed bone has been found in the soft parts of the body ; in the 
brain substance, dura mater, and pia mater ; in the pleura, diaphragm, 
and pericardium; in the skin, choroid, air passages, lungs, and penis, 
and in other places. To what extent some of these bone formations may 
have been due to inflammatory action it is not possible to say. 

Odontoma. — Tumors are sometimes formed from the pulp during the 
development of the teeth. When these contain dentin they are called 
odontomata. 

GLIOMA. 



The gliomata are developed from the characteristic framework of 
nerve tissue, the neuroglia, which in structure many, though usually not 
all, of its cells tlosely resemble. ^r^-^ 

Small cells with inconspicuous " " ^ 

bodies and numerous delicate 
branching processes are most 
characteristic ; but in connection 
with these there is usually a 
greater or less number of small 
spheroidal cells with proportion- 
ally large nuclei (Fig. 160). It 
is usually necessary to shake sec- 
tions in water or carefully tease 
fragments of the tumor in order 

to see the characteristic neuroglia or so-called ^^ spider ^^ cells (Fig. 161). 
These tumors may contain very numerous and frequently dilated thin- 
walled blood-vessels. They may be very soft or moderately hard ; and, 
especially when occurring in the substance of the brain, are frequently 




Glioma of Brain. 



298 



TUMORS. 



not sharply outlined against the adjacent normal tissue. They usually 
occur singly, and are comparatively slow in growth. 

They are frequently associated with other tumor tissue, forming glio- 
myxoma, glio-sarcoma, etc. Owing to the abundance of thin-walled blood- 
vessels and the softness of the 
growth, they are liable to inter- 
stitial haemorrhages, and may 
then, when occurring in the 
brain, readily be mistaken for 
ordinary apoplectic clots. They 
are liable to fatty degeneration. 
They usually occur in the brain, 
spinal cord, and in the optic and 
other cerebral nerves. The so- 
called gliomata of the retina are 
usually small spheroidal -celled 
sarcomata. 

Pure gliomata are benign 
tumors, though in their most 
common combination with sar- 
coma they may be very malignant. Their usual situation, however, is 
such as to make them almost always significant, although technically they 
are benign tumors. ^ 




Fig 



161. — Neuroglia or " Spider " Cells from 
Glioma of the Brain. 

Teased Specimen. 



MYOMA. 

Tumors composed of muscle tissue are of two kinds, following the 
two normal types of muscle, the non- striated and the striated. 

I. Leiomyoma, Myoma Levicellulare. — The characteristic elements of 
these tumors are fusiform, smooth muscle cells, with elongated or rod- 
shaped nuclei. These are packed closely together, frequently interlacing 
and running in various directions, and are intermingled with a variable 
quantity of more or less vascular fibrillar connective tissue (Fig. 162). 
When, as is not infrequently the case, the connective-tissue elements are 
present in large amount, the tumor is called fibro-myoma (Fig. 163). It 
is not always easy in sections to distinguish between these tumors and 
certain cellular fibromata, but the characteristic shape of the isolated 
cells and their nuclei, together with their uniformity in size, will usually 
suffice. These tumors are frequently infiltrated with lime salts, and, 
OAving to their density and lack of blood-vessels, they not infrequently 
degenerate, forming cysts or becoming gangrenous. They may occur 
singly or be multiple, are usually of slow growth, may be large or small, 
and are benign. They may occur wherever smooth muscle tissue exists. 
They are most frequently found in the uterus, where they are often mul- 

^ Our knowledge of the normal neuroglia is still too meagre to permit us to under- 
stand very thoroughly this class of tumors, and to separate it as precisely as could be 
wished from certain of its allies among the abnormal connective-tissue growths. See 
foot-note, p. 274. 



TUMOES. 



299 



tiple. They may occur in the wall of the gastro -intestinal canal, and 
have been seen in the kidney, in the bladder, and in the skin. The so- 








Fjg. 16;i.— Myoma ok the Ui\:rls. 

This is of the smooth muscle type— leiomyoma— and shows one bundle of muscle cells cut lengthwise, others 

across. 






^ 



^ 



called hypertrophies of the prostate, so frequent in advanced life, are 

sometimes considered leiomyomata of the interstitial muscle tissue of that 

gland. 

II. Myoma Striocellulare, or Rhabdomyoma. — In these rare tumors 

striated muscle fibres are the characteristic elements. They very rarely 

compose a great part of the tumor, 
but are intermingled with other ele- 
ments, fibrillar connective tissue, 
spindle-shaped and spheroidal cells of 
various forms, which often appear to 
be incompletely developed muscle 
cells. They are not infrequently 
associated with sarcomatous tissue. 
Blood-vessels and sometimes nerves 
are also present. The muscle fibres 
differ, as a rule, from normal striated 
muscle fibres in their arrangement, 
which is usually quite irregular, and 
also in size, being in general smaller 
than normal fibres, although varying 
greatly. The sarcolemma is either 
absent or incompletely developed. 
These tumors are usually small or 
of moderate size, and are supposed to 
originate from inclusions of cells 
destined to form muscle tissue in 
places where they do not belong. 
In the heart and certain other muscular parts small circumscribed 

masses of striated muscle tissue have been described, and are sometimes 




Fig. 163.— Fibro-Myo-Ma of Uterus. 

The muscle cells are crowded apart by dense 
fibrous tissue. 



300 



TUMORS. 



called homologous rhaMomyomata. But genuine heterologous rhcMomyo- 
mata are, in almost all cases thus far recorded, confined to the genito- 
urinary organs, kidney, ovary, and testicles. The writer has described 
an exceptional case of rhabdomyoma occurring in the parotid gland. ' 

These tumors, when not associated with other and malignant tumors, 
are benign and are of much greater theoretical than practical interest. 




Fig. 164.— Neuroma Ganglioniforme. 
Section from a tumor of the adrenal. 



NEUROMA. 

A true neuroma is a tumor containing new-formed nerve tissue. Such 
tumors are comparatively rare. Tumors developed in the connective 

tissue of nerves and composed 
usually of fibrous or mucous 
tissue are common, and are fre- 
quently called neuromata, but 
they should be called fibromata 
or myomata, etc. , of the nerA^es, 
or false nein^omata. The true 
neuromata are of two kinds, 
ganglionic or cellular neuromata 
Bjiid fibrillar neuromata, depend- 
ing upon the character of nerve 
tissue which they contain. 
The ganglionic neuromata — 
neuroma ganglioniforme — in 
which new-formed nerve cells are present (Fig. 164), are found asso- 
ciated with other structures in certain of the teratomata in the ovaries, 
testicles, and in the sacral region ; they also occur in the gray matter of 
the brain. They have been found in the adrenals. 

The fibrillar neuromata are, according to Virchow, of two kinds, mye- 
linic and amyelinic, depending upon whether the nerve fibres which they 
contain are meduUated or not. The neuroma myelinicum is the more com- 
mon and the best understood. The medullated nerve fibres in these 
tumors are associated with fibrillar connective tissue, and are usually 
curled and intertwdned in a most intricate manner. They are either sin- 
gle or multiple on the peripheral nerves. They may occur in consider- 
able numbers as nodular tumors on the branches of a single nerve trunk, 
or they may form an irregular, diffuse, nodulated enlargement of the 
nerve branches — plexiform neuroma. These neuromata may or may not 
be painful. They not infrequently form at the cut ends of the nerves 
in amputation stumps. They are benign tumors, never forming metas- 
tases. 

The false neuromata are myxomata, or fibromata (Fig. 165), or some- 
times myxo- sarcomata of the nerve sheaths or intrafascicular connective 
tissue, and may be single or multiple. In the latter case they may affect 

1 American Journal of the Medical Sciences, vol. Ixxxv., p. 438, 1883. For later 
bibliography consult Helhing, Centralbl. f. Path., Bd. ix., p. 433, 1898. 



TUMOES. 



301 



the branches of a single nerve trunk (Fig. 166), or thej may be found 
on nearly all the cerebro -spinal peripheral nerves. The writer has de- 
scribed a case (Figs. 166 and 167), in which more than eleven hundred 




Fig. 165.— False Neuroma— Fibroma of Lumbar Nerve. 

The fibrous tissue is loose in texture and in places oedematous, so that many of the nerve flhres pass through 
the tumor with little structural alteration. 

and eighty-two distinct tumors were found distributed over nearly all 
the peripheral nerves of the body. ' 

The nerve fibres in these tumors may be crowded apart by the new 
growth and considerably atrophied ; or, in cases in which the tumor is 
composed of soft tissue, as in myxoma or the soft fibroma, they may 




Fig. 166.— Multiple Fibromata (False Neuromata) of Pxeumogastric Nerte. One-quarter natural 

size. 

From the same case as that from which the photographic reproduction of Fig. 167 is made. 

pass through or around the tumor entirely unchanged. The multiple 
false neuromata are in many cases congenital. 



ANGIOMA. 

Angiomata are tumors consisting in large part or entirely of new- 
formed blood- or lymph-vessels or cavities. In many tumors of various 
kinds the new-formed or the old blood- and lymph -vessels may be very 
abundant or prominent by reason of their dilatations; the vessels of 
otherwise normal tissues may also be largely dilated, thus simulating 

^ Prudden, American Journal of the Medical Sciences, vol. Ixxx., p. 134, 1880. 
Consult also Preble and Hektoen, Trans. Assn. Am. Plij^s., vol. xv., p. 470, 1900 bibl 



302 



TUMORS. 




Fig. 1B7.— Multiple Fibromata- 



False Neuromata— OF the Peripheral Nerves of the Arm and 
Leg. 



A , Nerves of the right arm : B, the left sciatic with its branches ; C, the left anterior crural with its 
branches. From the same case as Fig. 166. The nerves of the other extremities were similarly involved. 



TUMORS. 



303 



vascular tumors. These are, however, not true angiomata, although 
sometimes reckoned among them, and in many cases closely allied to 
them. Such are the so-called arterial varix, or cirsoid aneurisms, and 




Fig. 168.— Angioma Telangiectoides from the Skin. 
This section is from a vascular naevus, " strawberry mark," of the skin. 

haemorrhoids, and various lymphectasise. True angiomata are of two 
kinds— I. Hsemangioma, and 11. Lymphangioma. 

1. Hsemangioma. — These tumors are of two types: 1. Those formed 
largely of capillary blood-vessels with either thin or thickened walls, 
embedded in a more or less abundant connective-tissue stroma. These 
are called simple angiomata or angioma telangiectoides (Fig. 168). The 
walls of the vessels in these 

tumors are frequently dilated 
or pouched, and usually form 
a tangle of curled and inter- 
twined vessels. They occur 
most frequenUy in the skin 
or subcutaneous tissues, usu- 
ally about the face, and may 
project above the general sur- 
face or be on a level with it. 
Such are the so-called vascu- 
lar ncevi, or straicberry marks, 
which are usually congenital. 
They are sometimes sharply 
circumscribed, and sometimes 
merge imperceptibly into the 
surrounding skin. They 

sometimes occur in the mucous membranes, in the mamma, bones, and 
brain. They are benign tumors, never forming metastases, but may be 
associated with sarcomata. 

2. The second form of hsemangioma, called angioma cavernosum (Fig. 




Fig. 169.— Angioma Caternosum of Liter, 
This section shows the entire small tumor. 



304 



TUMORS. 



169), consists largely of a series of iutercommunicating, irregular -shaped 
larger and smaller blood spaces lined with endothelium, and surrounded 
by a variable quantity of fibrillar connective tissue, which may contain 
smooth muscle cells. They resemble the erectile tissue of the corpora 
cavernosa of the penis and clitoris. They are apparently formed by a 
dilatation of old and new-formed capillaries and veins. They are some- 
times erectile and sometimes pulsating, and' are not infrequently multi- 
ple. They may be seated in the skin and subcutaneous tissue forming 
the so-called projecting nsevi, or in internal organs. They are often 



^V 



•y 



74 



Fig. 170,— Congenital Lymphangioma from Arm of Child. 



found in the liver and less frequently in bone, the brain, spleen, uterus, 
kidney, intestines, bladder, and muscles. They are usually of little sig- 
nificance, though they may give rise to hemorrhages. 

II. Lymphangioma. — These tumors consist of dilated lymph channels, 
which either i^reserve approximately the general shape of the original 
lymph -vessels, or are distinctly cavernous in character (Fig. 170) or even 
cystic. They probably originate in part in new-formed, in part in old 
lymph channels. A strict distinction between tumors formed by a dila- 
tation of pre-formed and new-formed lymph channels is not possible, 
owing to the very primitive character of some of the ultimate lymph 
spaces and our lack of knowledge of their exact relations to adjacent 
parts. 

In the lymphangiomata there may be niuch or little connective tissue 
between the dilated channels, which are usually filled with a translucent 
or milky fluid resembling normal lymph. These tumors are usually con- 
genital, but are sometimes acquired. They usually occur in the skin as 
soft, sometimes considerably, sometimes but slightly elevated growths, 
and may occur in the tongue — some forms of so-called macroglossia. 
They are benign tumors, but may rupture, giving rise to serious lym- 
ph or rhoea. 



TUMORS. 



305 



Tumors in Which Epithelial Cells are Predominant or Char- 
acteristic Elements — Epithelial Tumors. 

I. ADENOMA. II. CARCINOMA. 

General Considerations Begarding Upithelial-Cell Tumors. 

While in the main, in the normal body, the general distinctions 
between epithelial and other tissues are fairly well marked, there are 
instances, esi)ecially those in which epithelial tissues are in process of 
physiological growth or rejuvenation, in which the distinctions are quite 
ill-defined. When we remember the rapid growth of many tumors, the 
tendency to incomplete formation of their cells, their diverse seats, and 
the various complicating conditions under which they originate and de- 
velop, it does not seem strange that the exact limitations of this class of 
tumors are not easy to fix, nor that they seem sometimes to merge into 
one another and into tumor tissues belonging to other classes. If epi- 
thelial cells, under all circumstances, had a definite and characteristic 
structure, or if, on the other hand, we could always know whether a 




Fig. 171.— Carcinoma of the Stomach— Medullary Carcinoma or Carcinoma Molle. 



given cell group originated in epithelium or not, the matter of distin- 
guishing l^etween tumors of- this and other classes would be simple and 
easy enough. As it is, in some cases both mori^hological and histogenetic 
criteria fail us, and the clinical history and gross appearance are not 
characteristic. Such instances — which are indeed rare — suggest the 
i:)ossibility that the facts at our command do not justify such definite 
distinctions between epithelial and certain other tumors as on both the- 
oretical and practical grounds we should like to command. While 
these difficulties in special cases must be acknowledged, the distinctions 
are in the main definite enough, and very useful both for clinical and 
scientific purjioses. 
20 



306 



TUMOHS. 



Epithelial tumors always contain, in addition to the more or less 
characteristic cellular elements, a connective-tissue stroma which gives 
them support and carries the vessels (Fig. 171). This stroma may be 
sparse or abundant, may contain few or many cells, is sometimes ar- 
ranged in irregular fascicles or bands, and very frequently forms the 
walls of well-defined, variously shaped spaces or cavities called alveoli, 
in which the epithelial cells lie. The epithelial cells, in most cases, lie 
along the walls of the alveoli without an intimate connection with them. 
They are, moreover, packed together without more intercellular substance 
than the usual cementing material common to epithelial cell masses. In 




this lack of fibrillar intercellular substance within the alveoli, and in the 
loose relationship between the cells and the alveolar walls, lie in many 
cases the chief morphological distinctions between certain carcinomata 
and alveolar sarcomata. 

In certain of the epithelial tumors there is a reproduction of typical 
gland tissue of various kinds, depending upon the seat and conditions of 
growth of the tumor. Such tumors are called 6ffZ^womofto (Fig. 172). A 
simple hypertrophy of a gland, or an increase in its size by excessive 
growth of its interstitial tissue, does not constitute an adenoma. There 
must be an actual new formation of more or less tyj)ical gland tissue. 
This is not always or frequently of exactly the same character as the 
gland tissue in which it originates, and always exhibits a certain lack of 
conformity to the type in structure and mode of growth. The alveoli 
and ducts usually have a lumen and sometimes a membrana propria, but 
the cells may differ in shape from one another and from those of the 
gland from which they spring. 

Epithelial tumors in which there is no close conformity to a glandu- 
lar type, but an independent and atypical growth of epithelial cells in 
the meshes of an old or new-formed connective -tissue stroma, are called 
carcinomata (Fig. 171). 

It will readily be seen that there must be a border region between 



TUMORS. 



307 



the adenomata and carcinomata, where conformity to the glandular type 
merges into the lawlessness of growth characteristic of carcinomata. In 
this border region a certain degree of individual bias must be permitted 
in assigning a name to the new growth. In some cases a sharp distinc- 
tion cannot be made : or the tumor may share in the characteristics of 
both, and then we very properly make use of the term adeno- carcinoma 
or car ciyio- adenoma. 

I. ADENOMA. 

The structure of the cellular elements of these tumors, and their ar- 
rangement into acini and ducts, vary even more than do those of the 
normal glands whose types they follow. The acini usually possess a 
more or less well-defined lumen and membrana propria (see Fig. 172). 
The adenomata sometimes merge into the surrounding tissue, or are con- 
tinuous with the gland tissue in which they originate ; sometimes they 
are distinct in outline and encapsulated. The interstitial tissue is some- 
times abundant, sometimes sparse, and may contain few or many cells. 
The irregularities of their growth often lead to the stoppage of the 




Fig. 173,— Adenoma op Stomach. 
A form of tumor which is on the border line of carcinoma and might be called adeno-carcinoma. 



lumina of their ducts and the formation of cysts. They may undergo 
mucous metamori)hosis and may become sarcomatous. 

Adenomata occur in the mamma, ovary, liver, kidney, thyroid, sali- 
vary and lachrymal glands, and in the caruncle ; in the mucous mem- 
brane of the nose, pharynx, stomach, intestine, and uterus; and occa- 
sionally in the sebaceous and sweat glands of the skin. The so-called 
multilocular cystomata of the ovary are among the most important of the 
adenomata. 

There are numerous papillary and polypoid growths, in gland ducts 
and on mucous membranes, in which there is an actual new formation 
of gland epithelium ; but this is usually secondary to a primary growth, 
beneath the epithelial layer, of some other tissue, such as fibrous or 



308 TUMORS. 

mucous tissue, aud the new growth of gland epithelium simply keeps 
pace with the growth of the stroma which it covers. Such growths are 
sometimes classed among the adenomata, but do not, strictly speaking, 
belong there. 

Many of the adenomata are benign tumors, being slow of growth 
and localized, but there are very important exceptions. Some of the 
adenomata of the stomach and intestines belong to the most malignant 
of tumors in rapidity of local extension, in the formation of metastases, 
and the development of cachexia. Certain of the adenomata of the 
uterus, mamma, and thyroid are also very malignant. It should be re- 
marked, hoAvever, that, as a rule, the malignant adenomata are those 
which, in structure, lie close upon the border line between tumors of 
this class and carcinomata (see Fig. 173), and by such observers as in- 
cline to lay more stress upon clinical than morphological distinctions 
they are usually classed among the latter. 

II. CARCINOMA. 

The tumors of this highly important class are composed, as above 
stated, of a connective-tissue stroma, forming more or less well-defined 
communicating spaces or alveoli, in which lie variously shaped epithelial 
cells arranged in an atypical manner. The stroma, containing few or 
many cells, may be, especially in the advancing portions of the tumor, 
composed largely of the old connective tissue of the part. It may, how- 
ever, be entirely new formed. The cells which lie in the spaces or alve- 
oli sometimes bear a veiy close, but sometimes only a general resem- 
blance to epithelium (Fig. 171). 

Within the last twenty years the opinion has found general accept- 
ance that new epithelial cells in tumors, as well as under other conditions, 
normal and pathological, arise after embryonic life exclusively from old 
epithelium. 

The apparent occurrence of primary epithelial tumors in parts of the 
body in which epithelium is not normally present, as in bone and the 
lymph-nodes, has been recorded; but these may have been metastatic 
tumors, in which the primary growth was small and overlooked, or they 
may have been displaced embryonic remains, which, according to Cohn- 
heim's hypothesis (see page 269), would explain their heterologous oc- 
currence. These possibilities of error should be taken into the account 
in the apparently exceptional cases, and it is to be remarked that they 
are becoming less and less as our knowledge increases and our technical 
facilities for research improve. 

A considerable number of the tumors formerly described as heterolo- 
gous primary carcinomata are now known to be formed by proliferation 
of endothelium, or mesothelium, ' and hence to belong to another class — 
endothelioma — although sometimes considerably resembling the carci- 
nomata in structure. 

^ See reference Mi not, p. 274. 



TUMORS. 



309 



A great practical difficulty in the description, and, to beginners, in 
tbe recognition, of the carcinomata and their varieties, lies in the great 
diversity in shape which their cells present. It should be always borne 
in mind that the shape of cells depends in part upon their inherited ten- 
dencies in growth, which we cannot see under the microscope; but to a 
greater degree upon the varying conditions of nutriment and pressure 
in which they are placed during life. In the normal body these condi- 




Fjg. 174.— Carcinoma of the Hand. 
This tumor is of the epitheliomatous type and presents a large, rough, ulcerated surface. 

tious conform to a certain standard, so that cells of a given kind at a 
given stage of development are approximately similar. 

In tumors, however, the lawlessness and lack of fixed conditions in 
growth are such that we may have many young and atypical so-called 
indifferent forms of cells ; while even the adult forms may depart widely 
from normal shapes. Thus, in cylindrical-celled carcinomata there are 
many fully developed cells which are never cylindrical ; there are many 
others not fully developed which are quite indifferent in form, looking 
just like many other young cells. Finally, there may be in such tumors 
inflammatory processes through which young connective-tissue cells are 
formed, not to be distinguished individually from the atypical forms of 
epithelium. Thus it is that there is no morxDhologically characteristic 
^^ cancer cell, ^' as was formerly supposed. Some of them are typical and 
some not, and the more tyiDical may resemble normal epithelial cells, 



^^'- 



310 



TUMORS. 



and the atypical may look like young connective-tissue cells or even 
lymphocytes. It is in the topography, together with the general charac- 




FiG. 175.— Cancer Cells Infiltrating the Tissue Spaces in the Vicinity of a Tumor of the 

Mamma. 

From carcinoma mammffi. Somewhat diagrammatic. 

ters of the cells and the situation of the growth, that we must seek for 
the evidences of the nature of such tumors. 

The carcinomata are very x>rone to local extension, the advancing 
tumor cells in the periphery making their way through the lymph spaces 
and forming new foci (Fig. 175). Metastasis is of frequent occurrence 



CKi) t ^/^ 






^ .7 



n- 



1 ' 



'^ 



A% 



\)^ f) 









Fig. 176.— a Growth of Carcinoma Cells in a Lymph- Vessel near a Tumor. 
Such cell masses are liable to be detached and carried along the vessel, forming metastases. 

in some forms, and takes place chiefly, though not exclusively, through 
the lymph-vessels (Fig. 176), frequently involving adjacent or remote 
lymph-nodes (Fig. 177). The growth of the tumor cells in the lymph- 



<N'.^_. 



J 



TUMORS. 



311 



vessels, either in the immediate vicinity of the original tumor or follow- 
ing metastasis in a distant part of the body, may distend these so that 




Fig. 177.— Metastatic Carcinoma (Epithelioma) in a Lympii-Node. 
The primary tumor was in the vagina. The section shows at the right a small "■ epithelial pearl." 

on free surfaces like the pleura and peritoneum they form a whitish, 
elevated network. Transverse sections of such distended lymph-vessels 
are shown in Fig. 178. Secondary tumors are in the main similar in 
general structure to the primary foci, but may differ from them in vas- 
cularity and the abundance of the stroma, or in the shape of the cells. 




m^A'^' 



Fig. 178.— Metastatic Carcinoma in Lymph-Vessels of the Pleura. 

The primary tumor was in the liver. The sub-pleural lymphatics are widely distended with the tumor-cell 

masses. 



312 TUMORS. 

The carcinomata are, as a rule, malignant tumors, but the different forms 
vary much in this respect. 

Carcinomata are liable to fatty, colloid, mucous, and amyloid degen- 
eration, and are especially prone to ulceration (see Fig. 174), to haemor- 
rhage and inflammation (Fig. 179). They may become partially calcified, 



• JO 















C2? 









Fig. 179.— Exudative Inflammation in Carcinoma. 

Showing leucocytes In the stroma and in the epithelium. The epithelium is disintegrating, and in the 
small region shown in the cut the leucocytes are apparently acting as phagocytes in the softening and re- 
moval of the disintegrating epithelium. 

and are not infrequently combined with other forms of tissue in the 
mixed tumors. 

They are more frequent in the middle-aged and elderly than in the 
young, but they may occur at any age. Multiple primary carcinomata 
have been occasionally reported. ' 



Forms of Carcinoma. 

In certain carcinomata of the skin and mucous membranes, the cells, 
following the type of epithelium from which they arise, as they grow 
older are apt to become flattened or squamous ; these tumors are called 
Squamous or Flat-celled Carciiiomata, or simj^ly Epitheliomata. In another 
class of tumors, such as frequently occur in the gastro- intestinal canal 
and uterus, the cells are more or less cylindrical in shape, forming a 
palisade-like lining to the irregular alveoli; such tumors are called 
Cylindrical- celled Carcinomata, although here again many of the cells are 
not cylindrical at all, but may have a great variety of forms. There is 
a third and very common form of tumor, in which the epithelial cells 

' See Warthin, Jour. Am. Med. Assn., May 6th, 1899, bibliography. 



,^4^ 



JtSi)^. 



TUMOES. 313 

have no constant characteristic shaj^e, but vary as much as do the cell 
forms in the various glands of the body. Such tumors are conveniently 
classed together as Carcinoma simplex. 

In addition to these forms there are several others which depend for 
their characteristics upon various metamorphoses or degenerations, or 
uj^on the preponderance of one or other of the anatomical constituents of 
the growth. It will be most convenient to give a brief description of 
these various kinds, one after another, with the understanding that they 
are not absolute specific forms, but are simj)ly varieties which it is con- 
venient to recognize for clinical as well as anatomical purposes. 

Epithelioma. — These tumors occur in the skin and in the mucous mem- 
branes which are covered with squamous epithelium. The cells present 
all of the various forms which normally exist in these parts — the cuboidal 
and polyhedral cells of the rete Malpighii, as well as the more superficial 
flattened forms (Fig. 180). Frequently the spined cells, or so-called 
^" prickle cells, " are largely reproduced. Having to a certain extent the 
same life history as the cells in which they originate, many of the tumor 






-^^^^W ^ 












'^^fi^ 






*%-, 
^ 









Fig. ISO.— Epithelioma of the Xeck. 
Shows epitheKal pearls, spined cells, and reticular masses of variously shaped epithelial cells. 

cells become dry, thin, and horny, like the epidermis cells, as thev grow 
older ; and since their growth and changes often occui- within the old 
lymph spaces of the affected tissue or in the new -formed alveoli, the 
cells are sometimes packed together in si)heroidal, concentric masses 
called '-epithelial pearls" (Figs. 181 and 182), which may sometimes be 
seen with the naked eye upon or near the surface of the growth. 



314 



TUMORS. 




Fig. 181.— Epithelioma of Axillary Lymph-Node. 

This metastatic tumor was secondary to a large epithelioma of the back of the hand. The small cells 
with darker nuclei are the cells of the lymph-node. It shows the epithelial pearls in various stages of 
formation. 

The new epithelial cell groups may be large or small, may be sepa- 
rated by much or little stroma; often form reticular masses (Fig. 183), 








Fig. 183.— Epithelioma of the Skin, Showing Masses of Epithelial Pearls. 
Reproduced from photogi-aph. 



-.s-Ksifsat 



iily 



TUMORS. 



315 



and may infiltrate the tissues deeply or remain near tlie surface ; or may 
project above the surface, forming wart-like or papillary growths. These 






, 1 



"i r 'ti^ 



4 - 









Fig. 183.— Epithelioma of Skin. 
Showing reticular masses of epithelial cells with fibrous stroma. 

tumors frequently ulcerate on the surface (Fig. 174), and the skin about 
them is apt to become thickened (Fig. 184). 

Epitheliomata are most apt to occur in the skin, especially in those 
p^rts in which it becomes continuous with mucous membranes — lips, ex- 
ternal nasal openings, eyelids, labia, and glans penis — and are frequent 
in the mouth, oesophagus, vagina, and about the cervix uteri. They 
may develop in congenital nsevi of the skin, such as that shown in Fig. 






WSMii: 









Fig. 184.— Epithelioma of Back of Hand. 

The flat tumor occupied nearly the entire back of the hand, and was ulcerating at the surface. The fig- 
ure shows the edge of the tumor and a portion of the ulcer. The papillge of the skin over the edge of the 
growth are hypertrophied, and the tissue about is infiltrated with small spheroidal cells. Fig. 181 shows a 
section from a metastatic tumor of the axillary lymph-node in this case. This tumor presented the gross 
appearance shown in the photographic reproduction in Fig. 17-i. 



316 



TUMOES. 



185. This occurrence illastrates a congenital local predisposition to tu- 
mor formation. Simple congenital nsevi are sometimes mistaken for epi- 
theliomata because of similarity in the gross appearance of certain forms. 










iy^l- 



',K-^ .- , ~- 



mm^^^' 



Fig. 185.— a Portion op a Congenital Njsvus of the Skin. 

Such small naevi are sometimes mistatan for epitheliomata and occasionally afford a starting-point for the 

latter. 

There are also carcinomata of the skin, composed of cuboidal cells ar- 
ranged in tubules or masses, which do not follow the type of the epithe- 
lium of the skin, but rather that of the sweat glands or sebaceous glands. ' 














10. 






Fig. 186.— Epithelioma of the Nose. 
Showing a small portion of the growth highly magnified. 

These tumors are found most frequently on the nose and eyelids (Fig. 
186) ; some of them resemble endotheliomata (Figs. 187 and 188). 

^ For a study of gland-like epitheliomata of the skin see Krom])echer, Ziegler's 
Beitr., Bd. xxviii., p. 1, 1900. 



:::^r- 



TUMORS. 317 

Sometimes certain of the cells in an epithelioma appear to coalesce, 
forming a large multinuclear mass. This variety of epithelioma is some- 
times called giant-celled epithelioma. 

Flexner' has described a rare tumor arising from the epithelial layers 
of the retina, which he calls a neuro-eioitheliomia. 

Epitheliomata are apt to recur if not thoroughly removed, and may 
form metastases, but in general they are the least malignant of the car- 



FIG. 187.— SMALL EPITHELIOMA OF THE SKIX OF THE FACE. 

cinomata. Some of the smaller forms may exist for years with no evi- 
dent tendency to growth (Figs. 187 and 188). 

Cylindrical-celled Carcinoma. — These tumors, closely allied to some 
forms of adenoma (see Fig. 173), occur in the stomach, intestines, and 
uterus. The cells may be only in part cylindrical, the remainder having 
various shapes, and all being loosely or closely packed in larger or smaller 
alveoli. They may have much or little stroma. They merge impercept- 
ibly into the next class : 

Carcinoma Simplex. — These, which are by far the most frequent of the 
carcinomata of internal parts, are characterized by the alveolar structure 
and by the absence of any special characteristic shape in the cells, which 



Fig. 188.— Small Superficial Epithelioma of the Face. 

may be spheroidal, polyhedral, fusiform, or cuboidal. They may or 
may not resemble the epithelium of the gland in which they originate. 
They are usually nodular tumors, and may be hard or soft. If the new- 
formed stroma is abundant and dense, and preponderates over the cellu- 
lar elements, the tumor is usually hard and is called scirrhiis or Jibro- 

1 Flexner, "A Peculiar Glioma (neuro-epithelioma) of the Eetina," Johns Hopkins 
Hospital Bulletin, August, 1891. 



318 TUMORS. 

carcinoma (Fig. 189). 11 on the other hand, the cellular elements largely 
preponderate, the tumor is usually soft, and, if it do not contain too 
many blood-vessels, may have a general resemblance to brain tissue, and 
is then called encephaloid or medullary cancer ; or, better, Carcinoma molle 
(Fig. 171). These are among the most malignant of the carcinomata. 



Fig. 189.— Fibro-Carcinoma or Carcinoma Durum (Scirrhus Carcinoma). 

The intercellular tissue in these carcinomata may become so abundant 
as nearly to obliterate the cellular elements, but it is doubtful if they 
ever undergo spontaneous cure in this way. These tumors may be hard 
in one portion and soft in another. They may contain many blood- 
vessels, C. telangiectoides. They occur as primary tumors in the mamma, 
stomach, liver, thyroid, salivary, and prostate glands, in the pancreas, 
kidney, testicle, and ovary, and may occur elsewhere. 

Gelatinous Carcinoma. — The cells of certain carcinomata, especially of 
the gastro- intestinal canal, may develop a translucent gelatinous material 
whose nature is not well understood, which accumulates within the cells. ' 
In some cases this accumulation is moderate when the protoplasm of the 
cells may be more or less encroached upon by the translucent droplets of 
the gelatinous material ; but in other cases, over large areas the cells are 
partially or entirely destroyed, and replaced by the new material so that 



Fig. 190.- Carcinoma Gelatinosum — ''Colloid Cancer." 
From a tumor of the stomach. 

the alveoli of the tumor are distended by it, and their walls appear very 

distinct in the midst of the gelatinous substance (Fig. 190). In such 

cases the alveolar structure of the tumor is sometimes very evident to the 

^ These tumors are often called "colloid cancers," but the material which character- 
izes them is not true colloid. 



TUMORS. 



319 



naked eye, and these tumors are therefore often called alveolar carcinoma. 
Sometimes only a part of the tumor is affected in this way. 

Carcinoma Myxomatodes. — The cellular elements of carcinomata may 
suffer mucous softening, and thus larger and smaller cysts containing a 
mucous fluid are sometimes formed. To this type of metamorphosed 
tumor the above name is sometimes applied, but it more properly belongs 
to carcinomata in which the stroma is composed of mucous tissue (Fig. 
191). Such tumors are most fre- 
quently found in the gastro- intesti- 
nal canal and mamma. 

Melano-Carcinoma. — Tumors of 
this class are rare, and are character- 
ized by the i)resence of a variable 
quantity of black or brown pigment 
particles either in the stroma or in 
the cells. They are usually soft and 
malignant, and most frequently oc- 
cur in the skin. 







Fig. 191.— Carcinoma Myxomatodes. 
From a tumor of the mamma. 



MoLLTJSCUM coNTAGiosuM Is the desig- 
nation of small soft multiple growths of the skin, most frequent on the face, arms, and 
chest, and on the external genital organs. They are lobulated and contain cells simi- 
lar to those of the rete Malpighii. Within the cells and crowding the nucleus to one 
side, or free among the cells, are rounded or ovoid bodies which are believed by many 
to be protozoan parasites. 

Bibliography of Tumors. 

The most extensive and important work on tumors, containing a vast store of in- 
formation, is that of Rudolph Virchoic, "Die krankhaften Geschwlilste." It is not com- 
pleted and is somewhat old, but is still invaluable as a work of reference. A valuable 
bibliography and digest of recent observations on tumors will be found in Ziegler's 
" Lehrbuch der path. Anat. , " Bd. i. , last edition. An important resume on the malig- 
nant tumors in childhood, by Stern, may be found in the Deutsche med. Wochenschrift, 
June 2d, 1892, p. 494. "An Introduction to General Pathology," by Sutton, contains 
many suggestive facts about tumors drawn from comparative pathology. Current ad- 
ditions to the subject maybe found in the files of Lubarsch and Ostertag's "Ergeb- 
nisse," see particiflarly Luharsch, Jahrg. 1, p. 289, for a comprehensive summary; also 
for newer bibliography to 1899, AscJioff, Jahrg. 5, for 1898, p. 73. 



CHAPTER X. 

THE LESIONS INDUCED BY POISONS. 

Forms of Poisons. 

A POISON lias been commonly considered to be a substance wliich 
when introduced into the body from without is capable of inducing, by 
means other than mechanical, pathological alterations of function or 
structure, or both. But this conception of poisons as extraneous pre- 
formed substances has recently been greatly modified. For it has been 
learned that poisons may be formed within the body, either through the 
action of micro-organisms upon its Organic constituents or through the 
metabolism of the body cells themselves. 

It is thus convenient in considering the lesions induced in the body 
by poisons — toxic lesions — to place in one group those due to preformed 
extraneous poisons — exogenous jyoisons — and in another group those due 
to substances formed within the body — endogenous jwisoiis. 

It has furthermore been found convenient to make three classes of 
the endogenous poisons. First, those which are formed under the in- 
fluence of micro-organisms in the course of the acute infectious diseases 
and whose effects are most appropriately studied in that connection. 
These may be called endogenous poisons of infectious origin. Second, those 
which are formed under the influence of micro-organisms in the gastro- 
intestinal canal or elsewhere and absorbed into the body fluids. Third, 
those which are formed by the metabolism of the body cells themselves. 

To endogenous poisoning induced by either of the latter two classes 
of agents, the term onto- intoxication has been most commonly and most 
appropriately applied. 

As we have already studied the toxic lesions of the infectious diseases, 
we have only to consider here : 

First, the lesions induced by preformed or extraneous poison — ex- 
ogenous poiso7is ; and second, those due to the endogenous poisons which are 
concerned in the so-called auto -intoxications. ^ 

^ The limitation of the term auto-intoxication as it is here used is adopted from Mar- 
tins, who has written most clearly and suggestively upon the subject. See Martins, 
"Pathogenese innerer Krankheiten, " Heft 1 and 2, 1899-1900. 



THE LESIONS INDUCED BY POISONS. 321 



The Liesions Induced by Exogenous Poisons.' 

Sulphuric Acid. 

The effects of this poison vaiy with the amount taken and with its strength. Death 
usually occurs in from two to twenty -four hours after the ingestion of the concen- 
trated acid. A case of death within an hour is recorded. When the poison is less con- 
centrated or its effects are less intense, the patient may survive for months. 

The skin of the face about the mouth may be blackened and charred by the acid. 

The mouth and pharynx are of a grayish or blackish color, or are covered with a 
whitish layer, while the deeper tissues are reddened. Sometimes these regions escape 
the action of the poison. 

The larynx, trachea, and lungs are sometimes softened and blackened hy the acci- 
dental passage of the acid into them. This ma}^ take place even when the acid does 
not pass into the oesophagus. 

The cesophagus seldom escapes. It is colored grayish or blackish, softened, and the 
mucous membrane comes off in shreds. If life is prolonged, cicatrices and strictures 
are formed. The stomach may contain a blackish, pulpj- fluid, due to the action of the 
acid on mucus, blood, etc. It is coated on its internal surface with a black, sticky 
layer, beneath wiiich the mucous membrane is reddened. The mucous membrane may 
be blackened in patches or stripes. The organ may be contracted and the mucous 
membrane corrugated. Sometimes perforation takes place and the acid blackens and 
softens the adjoining viscera. In protracted cases cicatrices are formed and the organ 
is contracted. If the poison is dilute there may be only the lesions of chronic gastritis. 

T^iQhlood is sometimes thickened, syrupy, acid, and maj^form thrombi in the vessels. 

Fatty degeneration of the renal epithelium is mentioned by some authors. 

The body may be partially preserved from decomposition, owing to the action of 
the acid upon the tissues. 

The solution of indigo in sulphuric acid, commonly known as sulphate of indigo, 
produces the same lesions as sulphuric acid, and also stains the tissues with which it 
comes in contact of a dark-blue color. It is stated that an indigo-blue tint is often 
found in the mucous membranes after poisoning by pure sulphuric acid. 



Nitric Acid. 

Death may occur very soon after the taking of the poison, but is not usual until 
the lapse of several hours, and may not ensue for several daj^s or weeks. 

The surface of the mucous membrane of the mouth, pharynx, and oesophagus is cov- 
ered Avith yellow eschars wherever the acid has touched it. Beneath and around the 
eschars the tissues are congested and red. The poison may reach the oesophagus 
without acting on the mouth. The stomach contains a viscous, sanguinolent, yellow 
or greenish fluid. The mucous membrane is congested, red, swollen, softened, and 
ecchymotic. It is rarely perforated. The duodenum may be inflamed, and the inflam- 
mation extend to its peritoneal coat. The rest of the intestines usually escapes the 
action of the acid. 

The larynx is very frequently acted on by the acid. There are yellow eschars, 
congestion and swelling of the mucous membrane, sometimes oedema of the glottis. 
The trachea may be inflamed and the lungs congested. 

If the patient survive the first effects of the poison, chronic inflammation, cicatriza- 
tion, and contraction may occur. 

The acid nitrate of mercury, if taken in a concentTated form into the stomach, may 
induce the same lesions as nitric acid. 

^ For special precautions to be taken in the post-mortem examination in cases of 
suspected poisoning, see p. 38. 
21 



322 THE LESIONS INDUCED BY POISONS. 



Hydrocliloric Acid. 

In fatal cases death occurs on the average in about twenty-four hours. The lesions 
are in general similar to those produced by sulphuric and nitric acids, except that the 
eschars are usually of a whitish color at first, becoming, after a time, discolored and 
disintegrated. It is also more common to find false membranes on the inflamed surfaces. 

Oxalic Acid. 

In fatal cases death may occur within ten minutes (in one case it occurred in three 
minutes) or it may be delayed for two or three weeks. The period of death does not 
depend, as do in general the symptoms, upon the amount and concentration of the 
poison. 

The mucous membrane of the mouth, 'pharynx, and cesophagus is usually white and 
shrivelled, and easily peeled off, and may be covered with brownish vomit from the 
stomach. The oesophagus may be much contracted. The stomach is usually contracted 
and contains a dark-brow^n, acid, mucous fluid. The mucous membrane of the stomach 
may be pale, soft, and easily detached, sometimes looking as if it had been boiled in 
water. Sometimes it is red and congested; sometimes blackened and gangrenous; 
sometimes peeled off in patches. Perforation is of rare occurrence. If life be pro- 
longed the whitened condition of the mucous membrane is succeeded by congestion and 
inflammation. The small intestines may be inflamed. Inflammation of the pleura and 
peritoneum, and congestion of the lungs, are of occasional occurrence. In some cases of 
death from oxalic acid there are no w^ell-marked lesions. 

Potassium oxalate produces the same lesions as oxalic acid. 

Tartaric Acid. 

This acid is seldom used as a poison, but in large doses may prove fatal. The 
lesions in the cases observed were redness and inflammation of the mucous membrane 
of the gastro-intestinal canal. 

Potash, Soda, and their Carbonates. 

These substances are not commonly used as poisons with suicidal or homicidal in- 
tent, but may be taken by mistake. They may cause death in a few hours, or life may 
be prolonged for several weeks. 

The mucous membrane of the mouth, pharynx, cesophagiis, and stomach is softened, 
swollen, congested, and inflamed, or may be peeled off. It may be blackened from local 
changes in the blood. The mucous membrane of the laryn.v and trachea may also be 
swollen and inflamed. 

If life is prolonged for some time, cicatrices and strictures of the esophagus and 
stomach are apt to be produced as a result of the reparative inflammation. 

Ammonia. 

The vapor of strong ammonia may cause death from inflammation of the larynx 
and air passages. The strong solution of ammonia prodvices lesions similar to those of 
potash and soda. The larynx, trachea, and bronchi are frequently inflamed, and may 
be covered with false membranes. Fatal inflammation of the rectum and colon has 
been produced by an enema of strong solution of ammonia. 

Potassium Nitrate. 

Accidental poisoning sometimes occurs from large doses of this salt. In the ob- 
served cases there were intense congestion and inflammation of the stomach and intes- 
tines, and in one case a small perforation of tlie stomach existed. 



THE LESIOXS IIS^DUCED BY POISONS. 323 

For the effects of several infrequently employed salts of the alkalies and alkaline 
earths, which for the most part produce simple inflammation of the gastro-intestinal 
canal, we refer to special works on toxicology. 

Phosphorus. 

Poisoning by phosphorus is much more common in France and Germany than in 
this country. Some of the forms of rat poison, of which this is a frequent ingredient, 
and the ends of matches, are common media for its administration. It is more often 
used with suicidal than with homicidal intent. 

The post-mortem appearances vary according to the length of time which elapses 
before death, which may be from a few hours to several months. 

If death takes place in a few hours the only lesions may be those produced by the 
direct local action of the poison. The mouth, pharynx, and oesophagus usually escape. 
The stomach may be only slightly reddened, or there may be patches of inflammation 
and erosion. The contents of the stomach are often mixed Avith blood and may have 
the peculiar smell of phosphorus. There may be little bits of wood present when the 
poison has been taken from the heads of lucifer matches. It is said that the mucous 
membrane of the stomach may emit a phosphorescent light in the dark. 

If death does not ensue until after several daj^s the lesions are more marked. The 
bod}^ is usually jaundiced. There may be ecchymoses beneath the pericardium, pleura, 
and peritoneum, in the lungs, the kidneys, the bladder, the uterus, the muscles, and 
the subcutaneovis connective tissue, and bloody fluid in the visceral cavities. 

Cliromatolysis of the ganglion cells may occur. 

The heart and Tolnntary muscles, the walls of the blood-vessels, and the epithelium 
of the pulmonary air vesicles may be in the condition of fatty degeneration. The blood 
is usually dark and fluid. 

The stomach sometimes presents no very striking changes. There may be small 
circumscribed spots of inflammation, erosion, or gangrene, and occasionally perforation. 
The most constant change is albuminous and fatty degeneration of the cells which line 
' the gastric follicles. In consequence of this the mucous membrane appears thickened, 
opaque, of white, gray, or yellow color. The small intestine appears normal or is con- 
gested. 

The liver is found in different degrees of albuminous and fatty degeneration, and 
is often stained yellow from the jaundice. It is usually increased in size and of a gray- 
ish-yellow or light-yellow color, unless stained by the bile. Less frequently the 
centres of the acini are congested, or the entire liver is congested, or there are small 
haemorrhages in the liver tissue. The liver may be soft, flabby, and smaller than nor- 
mal. In the interstitial tissue of the liver and along the branches of the portal vein 
there may be marked infiltration with small spheroidal cells. 

The kidneys*often present albuminous and fatty degeneration of the epithelium. 
The mesenteric lymph-nodes may be soft and swollen from hyperplasia. 

Arsenic. 

This poison is very frequently employed with suicidal intent. Death may occur 
in a longer or shorter time from the direct irritative effects of the poison upon the 
gastro-intestinal canal, with the symptoms wiiich usually accompany the ingestion of 
irritant poisons; or it may occur with symptoms of collapse, or coma, or shock; or the 
symptoms may resemble those of cholera. The average time of death in acute fatal 
cases is about twenty hours, but death has occurred in tM^enty minutes and has bet^n 
prolonged for two or three weeks. 

The mouth, ijharynx, and esophagus may be inflamed, but are more frequently un- 
altered. The stomach may be empty or contain mucus mixed with blood. The arsenic, 
in substance, may be found adherent to the mucous membrane or mixed with the con- 
tents of the organ. It has, in rare cases, been found encysted in the stomach in consid- 
erable quantity. When invisible to the naked eye a microscopical examination of the 



324 THE LESIONS INDUCED BY POISONS. 

stomach contents will not infrequently reveal characteristic crystals of arsenious acid 
or some of its compounds. The stomach may be contracted and its mucous membrane 
corrugated. The entire inner surface may be red and inflamed, or there may be patches 
or streaks of inflammation or deep congestion. The inflamed and congested patches 
may be thickened and covered with false membrane mixed with larger and smaller 
particles or masses of the poison. Ulceration, perforation, and gangrene ai'e rare. 
Blood may be extravasated into the mucosa and submucosa, and with the congestion 
give the mucous membrane a very dark-red or brown appearance. Frequently the 
mucous membrane is studded with small petechise. Sometimes the arsenic is converted 
in the stomach into the yellow sulphide. There may be acute gastritis, even when the 
poison is absorbed by the skin or otherwise and not introduced into the stomach. The 
epithelium of the gastric glands may undergo granular and fatty degeneration. 

The entire length of the intestine may be congested and inflamed, but the action of 
the poison does not usually extend beyond the duodenum. In some cases the solitary 
lymph nodules, Peyer's patches, and the mesenteric nodes are swollen. Inflammation of the 
bladder nxidi peritoneum, and congestion and oedema of t\\Q brain, have been observed, 
but are neither frequent nor in any way characteristic. Fatty degeneration of the 
muscles, liver, kidneys, blood-vessels, and vesicular epithelium of the lungs 2ivA cliromatoly- 
sis of the ganglion cells may follow arsenical poisoning. 

Alterations in the spinal cord indicative of acute myelitis have been described by 
Popon^ as occurring in dogs poisoned with arsenious acid. 

The walls of the stomach and intestines and other parts of the body may be pre- 
served from decomposition for a long time after death by arsenical poisoning. 

It should always be borne in mind, in examining cases of suspected arsenical poi- 
soning, that death may be produced by arsenic and its compounds without any appre- 
ciable lesions. While in general it may be said that in the cases in which no lesions 
are discovered death has probably occurred soon after the ingestion of the poison, it 
should be remembered that death without lesions may exceptionally take place long 
after the usual time at which inflammatory changes commence. 

Compounds of arsenic, such as the chloride and sulphide, and the arsenite (Scheele's 
green, Paris green), are sometimes used for suicidal purposes, and produce lesions simi- 
lar to those of arsenious acid. Paris green is a favorite article in New York, particu- 
larly among Germans, for suicidal purposes. It is usually taken in considerable quan- 
tities, and is often found in the stomach after death. ^ 



Corrosive Sublimate. 

The mucous membrane of the month and throat may be swollen, inflamed, or have 
a grayish-white appearance. The msophagus may be swollen and white, or congested, 
or unaltered. The mucous membrane of the stomach is usually congested or inflamed, 
or there may be patches of softening, ulceration, or gangrene. Perforation is of rare 
occurrence. Small ecchymoses in the mucosa are not uncommon. Sometimes there is 
little or no change in the stomach. Sometimes the mucous membrane of the stomach 
is slate-colored from the deposition of metallic mercury from the decomposed salt. The 

^ Popon, "Ueber die Yeranderungen im Riickenmarke nach Yergiftung mit Arsen," 
etc., Yirch. Arch., Bd. xciii., p. 351. 

'^ It is advisable, in cases of suspected arsenic poisoning, particularly if the body 
has lain for some time, as in exhumations, to preserve not only all of the internal organs 
entire for the chemist, but also portions of the muscles (back, thigh, arm, and abdo- 
men), and also one of the long bones, preferably the femur, since arsenious acid and 
its compounds are quite diftusible, and may be present in proportionately larger quan- 
tity in other parts than in the gastro-intestinal canal. It is desirable to save the whole 
of the internal organs, and to weigh the muscle and bones as well as the whole body at 
the autopsy, in order that the calculations of the chemist, in case arsenic be found, may 
rest upon a definite basis, and be as little as possible dependent upon estimates, whose 
value may be questioned by lawyers should the case come into the courts. 

An interesting article on arsenic as a poison, with various collateral data by Pellew, 
will be found in Hamilton's "System of Legal Medicine," vol. i., p. 349. 



THE LESIONS INDUCED BY POISONS. 325 

intestines may appear normal, or there may be patches of congestion and ecchymosis. 
The larynx and trachea \\\a,y be congested. The kidneys may show albuminous and fatty 
degeneration of the epithelium. 

Lead. 

The different preparations of lead may prove fatal either from the immediate effect 
of large doses or from the gradual effects of repeated small doses. Although there may 
be marked symptoms during life, the post-mortem lesions are few and variable. 

There may be chromatolj^sis of the ganglion cells. 

Large doses may produce acute gastritis, and sometimes a wdiitening of the mucous 
membrane. The intestines are generally contracted, and there may be fatty degenera- 
tion of the renal epithelium; very frequently there are no appreciable lesions. 

In chronic lead poisoning the intestines may be contracted, the voluntarj" muscles 
flabby and light colored, or partially replaced by connective tissue, and there may be 
chronic meningitis. 

Copper. 

Acute poisoning by salts of copper is not very common, but it is of occasional acci- 
dental occurrence, and the salts are infrequently used with suicidal intent. The sul- 
phate and acetate are the most important salts in this respect. Soluble salts of copper 
may be formed in the use of copper cooking utensils, and accidents most frequently 
occur in this "way. 

The post-mortem appearances are somewhat variable. The pliarynx and (esophagus 
may be somewhat inflamed or unchanged. The mucous membrane of the stomach and 
intestines may be inflamed, ulcerated, or gangrenous, and perforation and peritonitis 
may occur. The mucous membrane may have a diffuse greenish color, or particles of 
the salt may be found adhering to it. 



Tartar Emetic. 

This preparation of antimony ma}^ prove fatal when administered in a single large 
dose or in repeated small doses. The post-mortem lesions are not constant. In cases 
of chronic poisoning there are usualh" no appreciable lesions. 

In cases of acute poisoning there may be evidence of acute inflammation of the 
(Esophagus, stomach, intestines, and peritoneum. Sometimes the stomach exhibits no 
lesions, while the intestine is involved. The larynx and lungs may be deeply congested. 



Vegetable Irritants. 

r 

Aloes, colocynth, gamboge, jalap, scammony, savin, croton oil, colchicum, veratria, helle- 
bore, elaterium, and turpentine. 

All these drugs may produce poisonous effects. The post-mortem lesions are con- 
gestion, inflammation, and sometimes ulceration of the gastro -intestinal mucous mem- 
brane ; but these lesions are sometimes present and sometimes absent. 



Cantharides. 

This substance may be given in poAvder or tincture. The entire length or only a 
portion of the alimentary canal may be congested or inflamed. There may be patches 
of gangrene of the mucous membrane of the stomach. When the poison has been taken 
in substance a microscopical examination of the contents of the alimentary canal or of 
the mucous membrane may reveal the glistening green and gold particles of the fly. 

The kidneys, ureters, and bladder may be congested and inflamed. There is some- 
times congestion of the brain and its membranes. 



326 THE LESIONS INDUCED BY POISONS. 

Opium and Morpliin. 

The post-mortem appearances in persons who have died from opium or morphine 
poisoning are inconstant and not characteristic. Congestion of the brain and its mem- 
branes, with serous effusion in the membranes and ventricles, and congestion of the 
lungs, are changes occasionally seen, but they are frequently entirely absent, and when 
present are not characteristic of death from this poison. , 

Poisonous Fungi. 

The action of these substances varies greatly, and the post-mortem appearances are 
inconstant and not characteristic. In general, when any lesions are present they are 
those of gastro-intestinal irritation or of venous congestion, or both. 

Microscopical examination may reveal characteristic fragments of fungi in the con- 
tents of the alimentary canal. 

Hydrocyanic Acid. 

This poison in fatal doses may destroy life in a very short time. The post-mortem 
appearances are inconstant and not characteristic. The skin may be livid and the mus- 
cles contracted. The stomach may be congested or normal. The most frequent internal 
appearances are those of general venous congestion. Under favorable conditions the 
odor of prussic acid may be detected in the stomach or blood or brain, or other parts of 
the body. It may be absent in the stomach and present in other parts of the body. If 
the patient have lived for some time the odor may be absent altogether. 

Cyanide of potassium may produce the same lesions as hydrocyanic acid, and there 
is the same inconstancy in their occurrence. 

Nitrohenzol. — This substance produces general venous congestion, and the odor of 
the oil of bitter almonds may be more or less well marked in the body after death. 

Carbolic Acid. 

"When this poison is taken into the stomach the mucous membrane of the mouth, 
oesophagus, 'And stomach Tuoij he white, corrugated, and partially detached in patches, and 
the edges of the affected parts may be hypersemic or there may be patches of extrava- 
sation. Brownish, shrunken patches may be present about the mouth. The brain and 
meninges may be congested. There may be congestion and oedema of the lungs, and 
congestion of the liver and spleen. The blood is usually dark and fluid. The urine is 
commonly of a dark or greenish color. The odor of the poison may be evident in the 
body and in the urine. 

Alcohol. 

The different preparations of alcohol, when taken in concentrated form or in large 
quantities, sometimes produce sudden coma and death in from half an hour to several 
hours. In acute poisoning, if death have followed soon after the ingestion of the poison, 
the body may resist decomposition for an unusual length of time. The stomach and 
tissues may even have a more or less well-marked alcoholic odor. The stomach, and 
even the oesophagus and duodenum, may be of a deep -red color. There may be jDuncti- 
form ecchymoses in the gastric mucous membrane. In many cases the stomach is ap- 
parently quite normal. There is apt to be venous congestion in some of the internal 
organs, but this is not constant. There are frequently congestion, and sometimes extrava- 
sation of blood in the brain and its membranes, and oedema of the membranes or of the 
brain substance, or both. There may be a serous effusion in the ventricles of the brain, 
also chromatolysis of the ganglion cells. 

In chronic alcohol poisoning death may ensue from some other disease, or after a 
debauch. In the latter case there may be delirium tremens, or the patient dies exhausted 
and comatose. Chronic alcoholism is not infrequently mistaken clinically for meningi- 



THE LESIOXS INDUCED BY POISONS. 327 

tis. The post-mortem lesions are sometimes marked, sometimes absent. There may be 
chronic pachymeningitis, resulting in thickening of the dura mater and its close adher- 
ence to the skull. T\\Q pia mater vciOij ha thickened and oedematous. The 5/Y«'r< may 
be normal or oedematous or atrophied and show chromatol3'sis of the ganglion cells. 
The lungs are frequently congested. The heart may be thickly covered with fat, and 
its walls may be flabby and fatt}'. The stomach frequently presents the lesions of 
chronic gastritis. The liver may be cirrhotic, with or without fatty infiltration. The 
kidneys may present the lesions of albuminous or fatty degeneration or of chronic dif- 
fuse nephritis. 

It should always be remembered, however, that all or a part of the above lesions 
may be absent in the bodies of drunkards, and, furthermore, that the same lesions may 
be due to other causes. 

Chloroform. 

Chloroform may cause death when it is taken in fluid form into the stomach or when 
inhaled. Death from swallowing liquid chloroform is rare, and its immediate cause is 
usually uncertain. The post-mortem changes are variable; sometimes there are no 
lesions. In some cases there is simple reddening of the gastric mucous membrane; oc- 
casionally there is acute gastritis or ulceration of the mucous membrane. The odor of 
chloroform may or may not be evident. Discoloration and softening of the mucous 
membrane of the pharynx, oesophagus, and duodenum have been observed. There may 
be general venous congestion ; the heart may be flabb^^ Bubbles of gas have been 
frequently seen in the blood, but this is not characteristic. Death from inhalation of 
chloroform is a not infrequent accident in surgical practice. After death from inhala- 
tion the results of the examination are usually quite negative. 

Ether. 

The inhalation of ether occasionally causes death. The post-mortem examina- 
tion is negative. The ingestion of fluid ether may induce inflammation of the stomach. 
The odor of ether may be perceptible if the autopsy is made soon after death. 

Chloral Hydrate. 

There are no characteristic post-mortem appearances after death by chloral. Hy- 
persemia of the brain, and the odor of the drug, have been noticed. 

Strychnin— Nux Vomica. 

The post-mortem appearances after poisoning by these drugs are not characteristic 
and are inconstant. The body is usually relaxed at the time of death, but the rigor 
mortis, as a rul^, comes on early and remains long. There may be congestion of the hrain 
and spinal cord, and sometimes of the lungs and stomach. Chromatolysis of the ganglion 
cells is recorded. 

Animal Venom, etc. 

The poisons which may be introduced into the bod}' through the bites of venomous 
snakes and reptiles and the bites of insects cannot be considered in detail here.^ 

Abrin and ricin are examples of poisonous substances which induce in the body 
lesions similar to those in certain infectious diseases (see page 178). 

Carbonic Oxide. 

This is one of the gases generated in the burning of charcoal, and forms one of the 
ingredients of illuminating gas. The most characteristic post-mortem appearance is 
the cherry-red color of the blood, and of the tissues and viscera which contain blood. 

^ Consult Langman, "Poisonous Snakes and Snake Poison," Medical Record, Sep- 
tember loth, 1900; also Broicn, "Twentieth Centur}- Practice," vol. xx., bibliography. 



328 THE LESIOXS INDUCED BY POISONS. 

The presence of carbonic acid in the gas may obscure the bright red of the carbonic 
oxide by tlie dark color wliicli it induces in the blood. 

Carbonic Acid. 

The lesions are essentially those of asphyxia, but the brain is said to be more fre- 
quently congested than in asphyxia by simple obstruction of respiration. 

Conium, Aconite, Lobelia Inflata, Digitalis, Stramonium. 

These vegetable poisons are administered in their natural form of leaves, berries, 
and roots, or in tinctures, infusions, and extracts, or in the form of their active alka- 
loid principles. 

If the leaves, berries, or seeds are given they may be detected in the contents of 
the alimentary canal by microscopical examination. Otherwise the results of autopsies 
are not characteristic. 

The hrain and its membranes, and the lungs, may be congested. The stomach may 
present patches of congestion, inflammation, and extravasation, or its entire mucous 
coat may be inflamed, or it m?ij appear normal. 

Ptomams and Other Putrefactive Products. 

Poisonous substances of various kinds are often developed in the putrefaction of 
organic substances, and certain alkaloidal substances called ptoma'ins form in the de- 
composition of proteids without putrefaction. Thus in sausages, some kinds of cheese, 
ice-cream, decayed fish and mussels, such substances have caused serious and even fatal 
poisoning. There are no characteristic post-mortem changes in poisoning by these sub- 
stances. But the lesions of gastro-intestinal inflammation or toxaemia may be present. 

These alkaloidal substances may be of extreme importance in certain cases of death 
from obscure causes on account of the medico-legal questions which may arise. ^ 

Bibliography of Endogenous Poisons. 

For a more detailed consideration of poisons, their effects, modes of detection, etc. , 
consult Taylor on Voi^on^; Jf«sc7iA;a'« " Handbuch der gerichtlichen Medicin," Bd. ii. ; 
Woodman and Tidy, "Forensic Medicine." Wormley's "Micro-chemistry of Poisons" 
contains a series of good plates of the microscopical appearance of various forms of 
crj^stals of poisonous substances. 

Lessees " Atlas der gerichtlichen Medicin " contains a series of colored plates show- 
ing the appearance of the stomach after the action of various poisons. The work of 
Guy and Ferrier on "Forensic Medicine," 7th ed., revised by Smith, contains in very 
compact and reliable form much information on the general subjects treated in the fore- 
going section. Leioin's "Lehrbuch der Toxicologic" contains many valuable and 
suggestive general considerations on the action of poisons. 



Lesions Induced by Endogenous Poisons— Auto- 
intoxications. 

As we turn now from poisons formed outside of the body to those 
formed within it — the endogenous i^oisons — we encounter at once two 
classes : I. Those poisons which arise from the metabolism of micro- 
organisms. II. Those which arise from the normal or aberrant metabo- 
lism of the body cells themselves. 

^ For chemical aspects of this subject consult Vaughn in Hamilton's "System of 
Legal Medicine," vol. i.,p. 475, and Vatighn and Novy, "Ptomams and Leucomains"; 
also Vaughn in "Twentieth Century Practice," vol. xiii. 



THE LESIONS INDUCED BY POISONS. 329 



I. ENDOGENOUS POISONS FORMED LARGELY UNDER THE IN- 
FLUENCE OF MICRO-ORGANISMS. 

1. Those which are formed in infectious diseases. (See Chapter 
Yin. , Part II. , on Infectious Diseases. ) 

2. Those formed in the body without infection. 

The most common and important metabolic poisons of this class 
are those which are formed in the gastro- intestinal canal through the 
action of micro-organisms, mostly bacteria, uj)on the organic constituents 
of the intestinal contents and secretions. The new chemical substances 
thus formed become deleterious when absorbed into the body fluids, and 
this may occur either when they are produced in unusual quantity or 
when their elimination with the excreta is interfered with. When ab- 
sorbed, some of these poisons may be demonstrable in the urine, and they 
may give rise to a variety of symptoms which cannot be considered here, 
but which are appropriately designated as marks of Enter ogenic auto -intox- 
ication. Such are dizziness, headache, some forms of tetany, gastro- 
enteritis, etc. 

Endogenous poisons analogous in origin with these may be formed in 
the bladder, in putrid abscesses, or in necrotic tissues in various parts 
of the body. Structural lesions, if such there be, occurring under these 
conditions are as yet but little known. 



II. ENDOGENOUS POISONS FORMED BY THE BODY-CELLS -HISTO- 

GENIC POISONS. 

It is only within the past few years that the studies on cell metabo- 
lism have led to the belief that the body cells may not only under occa- 
sional abnormal conditions form poisonous chemical comjDounds, but that 
even in the normal processes some of the intermediary metabolic prod- 
ucts may be inimical to the welfare of the body, if they be not constantly 
rendered ineft. This may be effected either by excretion or, as now seems 
probable, in part at least through the influence of what have been 
called the ^ internal secretions" of such glands as the thyroid, pancreas, 
adrenals, hypophysis, etc., or possibly in ways as yet wholly unknown. 

Thus there is a group of auto -intoxications due to the accumulation in 
the body of the products of normal metabolism through defects in the 
excretory apparatus, for example, uraemia in renal insufficiency or re- 
tention of urine ; cholaemia in retention of bile ; carbonic-acid i^oisoning 
in various forms and grades of asphyxia. Possibly some of the serious 
symptoms following extensive burns of the skin and occurring in sun- 
stroke and eclampsia are of similar origin. This may be called auto-intoxi- 
cation through retention. 

On the other hand, there is a group of auto-intoxications which it is 
assumed may in part at least be due to a failure of the organs concerned 
with the internal secretions to furnish the necessary link in the chain of 



330 THE LESIONS INDUCED BY POISONS. 

intermediary metabolic products. In this group may be placed cachexia 
strumipriva and myxoedema, pancreatic diabetes, Addison's disease, and 
possibly some forms of acute yellow atrophy of the liver. 

While the nature and action of the postulated internal secretions is 
still obscure, there is much reason to believe that they do indeed exist 
and are of extreme importance in the subtle adjustments of individual 
cell metabolism to the welfare of the organism as a whole, and that 
when this adjustment is disturbed, forms of histogenic auto-intoxication 
may arise. At any rate the hypotheses which have been formed in the 
new light have contributed largely to our understanding of a series of 
important general diseases. These diseases, whether involving or not 
internal secretions in accordance with our present conceptions, may be 
considered as dyscrasic auto -intoxications. ^ 

A¥hether gout, oxaluria, and some forms of simx^le diabetes should 
be considered as auto-intoxications may be questioned. Probably Base- 
dow's disease and some forms of puerperal eclampsia should be regarded 
as involving the formation and retention of histogenic poisons. 

Of course this grouping of diverse forms of disease should be consid- 
ered as only tentative and suggestive. And it may well be doubted 
whether analogy may not be often overstrained in regarding as the 
effect of i)oisons what may after all be metabolic aberrancies of far more 
subtle character than the word auto -intoxication would imj)ly. 

It should be borne in mind that in but a very small proportion of 
the abnormal processes which are considered auto-intoxications have the 
assumed poisons been actually demonstrated. The assumption rests 
largely upon symptoms which are regarded as analogous with those in- 
cited by known exogenous poisons. It is wise to remember also that 
even in poisoning by well-defined agents whose general effects have long 
been known we are almost totally ignorant, except in the case of the so- 
called destructive or corrosive poisons, of the exact ways in which they 
act. A few induce changes in the blood ; many appear to act upon the 
nerve cells ; but the nature of this action is still unknown. ^ 

Without insisting upon the advantage of such a grouping as has been 
outlined above, and with the full recognition of its incompleteness, the 
more important of the so-called ^^ general diseases," some of which may 
be regarded as auto -intoxications, will be considered in the next chapter. 

^ For a discussion of internal secretions, with bibliography, consult Transactions of 
the Congress of American Pliysicians and Surgeons, vol. iv., 1897. 

^ For convenience of reference the grouping of poisons briefly set forth above may 
be tabulated as follows : 

I. Exogenous poisons Inorganic and organic. 

' -c^ 1 . f A. In infectious dis- 

Endogenous poisons ^^^^^ 

formed largely hj\ b. Without infec t i o n , 
micro-organisms. | ^^^^^^^ enterogenic. 

Endogenous poisons formed under the influence of 
or by the body cells — histogenic poisons — induc- 
ts ing auto-intoxicaiioii in the more limited sense. 



II. Endogenous poisons — con- 
cerned in autochthonous or 
endogenic poisoning — auto- 
intoxication. 



CHAPTER XI. 

GENERAL DISEASES. 

CACHEXIA STRUMIPRIVA— MYX(EDEMA. 

The thyroid is one of the so-called ductless glands which are believed 
to furnish internal secretions essential to normal metabolism in the body. 

Eemoval or destructive lesions of this gland, both in man and the 
lower animals, ' may be followed by serious and fatal disease character- 
ized as Cachexia strumijyriva. In man the more common manifestation 
of this disease is called Myxcedema. It occurs most frequently in middle- 
aged women. 

The skin of the face is apt to be swollen and waxy, giving a peculiar 
and rather characteristic appearance to the features. The skin of the 
body is apt to be dry and rough, and the hair may fall out. Perspira- 
tion is, as a rule, diminished. The mental condition is dull, and loss of 
inemory and insanity may occur. Bodily movement and speech are apt 
to be imj)aired. The fat tissues may be atrophic, and the subcutaneous 
tissue has been shown in some, though not all, of the cases to contain an 
unusual amount of mucin. In some cases the fibres of the upper layers 
of the corium are crowded apart by fluid. 

The most marked and constant lesion in this disease is an atroj)hic 
condition of the thyroid gland. The parenchyma of the gland is more 
or less completely replaced by fibrillar connective tissue and by new- 
formed reticular tissue resembling the lymphatic tissue of the lymph 
nodes. Th^ general appearance of the atrophied thyroid gland is shown 
in Fig. 203. 

In addition to the lesion of the thyroid there are apt to be chronic 
endarteritis and chronic diffuse nephritis. In some cases there are an 
accumulation of small spheroidal cells about the smaller blood-vessels in 
various parts of the body, and also petechial haemorrhages. 

If the thyroid be completely removed in young animals there is defi- 
cient development of the osseous system, while in man the frequent asso- 
ciation of cretinism with goitre or other thyroid lesions indicates in 
another way the close relationshij) between the thyroid and cell metab- 
olism. ' The nature of the substances composing the internal secretions 
of the thyroid is little understood, but the wonderful therapeutic effects 

^For an extensive critical and experimental study of this subject see CunningMm, 
"Experimental Thyroidism," Jour. Exp. Med., vol. iii., p. 147, 1898, bibliography. 

- Consult Oder, " Sporadic Cretinism in America, " Trans, of the Congress of Ameri- 
can Physicians and Surgeons, vol. iv., p. 169, 1897. 



332 GENERAL DISESSES. 

of the administration of the extract of the gland in cases of myxcedema 
and in cretins make clear their great importance. Whether directly 
toxic snbstances are formed in the thyroid or not, it seems proper to con- 
sider the cachexia strumipriva as due directly or indirectly to anto -intox- 
ication. 

EXOPHTHALMIC GOITRE. (Basedow's Disease, Graves' Disease.) 

The characteristic lesions of this disease are unilateral or bilateral 
enlargement, largely hypersemic, of the thyroid gland and protrusion of 
the eyeballs — exophthalmos. These lesions are apt to be associated with 
functional disturbance of the heart. ' There is reason to believe that this 
condition may be due to hypersecretion of the thyroid gland, and that 
its functional characteristics may be properly regarded as indications of 
an auto -intoxication. 

ADDISON'S DISEASE. 

This name is apj)lied to a disease Especially characterized morpholog- 
ically by a peculiar pigmentation of the skin and by certain changes, 
morphological or functional, in the adrenals. The patients suffer from 
cerebral symptoms, great prostration, syncope, and derangements of the 
functions of the stomach and intestines. 

The pigmentation of the skin is the symptom which has especially at- 
tracted attention. The change in color usually begins and becomes most 
marked in those parts of the skin which are not covered by the clothing 
or are naturally of darker color. The rest of the skin afterward changes 
color, but not uniformly, white patches being left. The color is at first 
a light yellow or brown ; this becomes darker until it is of a dark green- 
ish, grayish, or blackish-brown. The mucous membrane of the tongue, 
lips, and gums may be similarly pigmented. 

Under the name of Addison's disease different observers have de- 
scribed cases in which the symptoms and bronzed skin existed without 
disease of the adrenals ; cases in which the bronzed skin was the only 
lesion ; and cases in which the adrenals were diseased without symptoms 
or bronzed skin. 

The Skin. — The discoloration of the skin is due to deposit of yellowish- 
brown j)igment in the deeper layers of the epidermis, especially in the 
layer covering the papillae, and less constantly in the connective tissue 
of the cutis. 

The Brain. — Pigmentation of the gray matter, acute meningitis, 
chronic meningitis, and distention of the ventricles with serum have been 
observed. 

The Sympathetic Nerves, especially those which are in contact with the 
adrenals, may show a variety of changes apparently due to chronic in- 

^ On the relationship between the thyroid and Basedow's disease, consult Eiilenherg, 
Deutsche med. Wochensch., October 4th, 1894; also Edmunds, Jour, of Pathology and 
Bacteriology, vol. iii., p. 488, 1896; Fariier, Virchow's Archiv, Bd. cxliii., p. 509, 1896, 
bibliography. 



GENEEAL DISEASES. 333 

flammation. Various changes in the nerve cells of the semilunar ganglia 
have been described. 

The Heart. — The muscle fibres may be the seat of fatty degeneration. 

The Adrenals. — The most common lesion of these bodies is a tubercu- 
lous inflammation, and this or some other lesion has been found in nearly 
one-half of the cases. On the other hand, it should be remembered that 
similar lesions of the adrenals often occur without other indications of 
Addison's disease. Tuberculous adrenals may be large, hard, and nodu- 
lar ; less frequently of normal size or smaller than normal. On section 
they may contain cheesy masses surrounded by zones of gray, semi-trans- 
lucent tissue. Later the cheesy masses may become calcified or they may 
soften and break down. The grayish zones are composed of tubercle 
tissue, or denser connective tissue. 

Other cases have been described in which the adrenals were the seat 
of carcinoma or of fatty or waxy degeneration. But these lesions, esi)e- 
cially carcinoma of the adrenals, may occur without the manifestations 
of Addison's disease. The adrenals in some cases appear normal or they 
may be atrophied. ' 

On the whole the clinical, morphological, and experimental data now 
available seem to point to lesions of both the sympathetic system and 
the adrenals as of probable significance in determining this disease. 

The hypothesis which is most in favor at j^resent assumes that the 
adrenals furnish an internal secretion without which normal metabolism 
cannot be effected, and that lesions of the adrenals or of the sj^mpathetic 
ganglia and vessels about them, by altering or diminishing this secretion, 
may lead to the functional and structural changes characterizing the 
disease. The propriety of considering Addison's disease as an example 
of auto -intoxication can hardly be decided in the light of the facts yet at 
our command. It is clear, however, that the adrenals contain very pow- 
erful chemical substances which have a marked effect upon certain tissues 
of the body. ^ 

DIABETES MELLITUS. 

This disease involves such defects in nutrition as lead to an abnormal 
accumulation of sugar in the blood and its discharge by the urine, which 
is increased in amount. 

A great variety of lesions have been found in the body after death 
from diabetes, but none of them and no combination of them appear to 
be of well-defined significance in this special relationship. The general 
condition of malnutrition and debility, so often marked in this disease, 
renders diabetics especially vulnerable to slight injuries or infections; 

^ For observations on the effects of removal of suprarenal body see Tizzoni, Ziegler's 
Beitrage, Bd. vi., p. 3, 1889. For recent and general bibliography consult Luharsch, 
"Ergebnisse d. spec. path. Morphologic u. Physiologic," Jahrg. i., Abth. 3, 1896, p. 
488; also the larger works on the practice of medicine. 

^ Consult, for bibliography concerning the effects of adrenal extract, Bates, Internat. 
Med. Mag., December, 1900. 



334 GENERAL DISEASES. 

gangrene, for example, is liable to occnr either with or without marked 
injury in eases of diabetes.' 

The Brain may appear to be entirely normal ; it may be congested ; 
there may be an increase of serum; the convolutions may be shrunken; 
there may be meningitis ; there may be dilatation of the blood-vessels, 
small extravasations of blood around the vessels, enlargement of the peri- 
vascular spaces, and alterations in the perivascular sheaths and nerve tis- 
sue bounding the cavities ; there may be tumors at the base of the brain. 

The Spinal Cord may present dilatation of the blood-vessels ; dilatation 
of the central canal ; changes in the gray matter of the anterior cornua. 
Marks of multiple neuritis and lesions of the sympathetic ganglia may 
be present. 

The Lungs, — There may be the lesions of pleurisy, bronchitis, broncho- 
pneumonia, lobar pneumonia, gangrene, tuberculosis. 

The Heart may be small or hypertrophied ; there may be chronic 
endocarditis. 

The Stomach and Intestines. — The stomach may be dilated, its walls 
may be thickened, there may be hsemorrhagic erosions of the mucous 
membrane. In the intestines there may be tuberculous ulcers or enteritis. 

The Liver may be cirrhotic or fatty, or glycogenic infiltration may 
occur. 

The Kidneys may be enlarged ; they may be the seat of albuminous 
degeneration or diffuse nephritis ; there may be glycogenic infiltration 
of the epithelium of Henle's loops. 

The Blood. — In a few cases fat has been found in the blood, and fat 
emboli in the vessels of the lungs. 

The Pancreas. — In a considerable proportion of cases the examination 
of the pancreas reveals some lesion, usually atrophy of the parenchyma, 
often with increase of the interstitial tissue. Fatty degeneration, tumors, 
and cysts have been found. Extirpation of the pancreas in man or dogs 
may lead to diabetes. While diabetes may occur without demonstrable 
lesions of the pancreas, it is fair to assume that functional lesions of 
grave importance may nevertheless be present. ^ 

Diabetes mellitus may be associated with haemachromatosis and cirrho- 
sis of the liver — so-called ^^ bronzed diabetes. '' ^ 

Under the influence of the doctrine of internal secretions it is now 
commonly assumed that the pancreas in addition to its intestinal secre- 
tion furnishes other substances to the body which are essential in the 
metabolic changes to which the carbohydrates and proteids must be sub- 
jected in securing normal nutrition. Interference with this internal se- 
cretion of the pancreas is thus assumed to be accountable for the faulty 
metabolism. " 

^ For bibliography of diabetic gangrene consult Davis, Jour. Am. Med. Assn., July 
16th, 1898. 

'^ For bibliography of diabetes consult Von JSloorden, " Twentieth Century Practice, " 
vol. ii. 

^See Oipie, Jour. Exp. Med., vol. iv., p. 292. 

'^ Other forms of glycosuria are known which are to be otherwise accounted for, and 



GENERAL DISEASES. 335 



GOUT. 



The characteristic lesion of gout is the presence of an abnormal 
amount of uric acid in the blood and the deposit of urate of sodium in the 
articular cartilages, the ligaments of the joints, the ears, and the eyelids. 
Inflammatory changes may be associated with the dei)Osits in the joints. 

The most frequent situation of the gouty deposit is the metatarso- 
phalangeal joint of the great toe. The cartilage may be infiltrated or 
encrusted with the deposit. These masses of urates, often called '^ chalk- 
stones,^' may appear upon the surface by the ulceration of the skin. 

A very important feature of gout is that patients with the gouty di- 
athesis are especially liable to derangements of digestion and to certain 
chronic inflammations, such as chronic inflammation of the arteries, the 
bronchi, and the kidneys. Cardiac hypertroj)hy may be associated with 
the arterio- sclerosis. The interstitial tissue, especially in the pyramids 
of the kidney, may be infiltrated with the urates. 

It is not yet clear whether the accumulations of uric acid in the body 
in gout is due to faulty elimination or to local alterations which favor its 
deposition, ^ov is the relationship plain of local inflammatory processes 
to the gouty deposits. 



SUNSTROKE. (Insolation; Heat Exhaustion.) 

Persons exposed while at work or when exhausted to the sun or to 
high temperatures are liable, especially if of intemperate habits, to sud- 
den prostration, often associated with cardiac failure, asphyxia, convul- 
sions, and coma. Death in many cases soon ensues. 

After death, decomposition sets in early and progresses rapidly. The 
blood usually remains fluid. 

The brain and its membranes are in some cases congested, in others 
not. There may be an increased amount of serum beneath the pia mater, 
or small and thin extravasations of blood beneath the pia mater and be- 
tween the pia and dura mater. Chromatolysis of the ganglion cells has 
been described by Yan Gieson' and others. The thoracic and abdominal 
viscera may be congested ; albuminous degeneration may be evident in 
the liver and kidneys. 

In the cases in which cerebral symptoms are protracted for a number 
of days the lesions of meningitis have been found after death. 

According to Cramer, ^ persons surviving for some time the first severe 
effects of the heat may suffer important alterations in certain nerve fibres 
of the brain, 

whicli may be associated with lesions of the nervous system or induced by the action 
of certain poisons, phloridzin-diabetes, for example. 

1 Van Gieson, "Toxic Basis of Neural Diseases," N. Y. State Hospitals Bulletin, vol. 
i., p. 407, 1896; also Lambert, Medical News, July 24th, 1897. 

'^Cramer, Centralblatt fiir allg. Path., etc., Bd. i., p. 185, 1890. 



336 GENERAL DISEASES. 



SCORBUTUS. (Scurvy.) 

This disease appears to result from imperfect nutrition under condi- 
tions which cannot be considered in detail here, but which is usually at- 
tributed to insufficient or inappropriate diet. Tne lesions are variable, 
the most prominent being anemia ; extravasation of blood in the skin, 
sul^cutaneous tissue and muscles ; swelling and ulceration and bleeding 
of the gums. Small and sometimes extensive hsemorrhages are apt to 
occur in the mucous membranes and on serous surfaces. Small ulcers 
may form in the mucous membranes. Fatty degeneraton of the heart, 
liver, and kidneys is not uncommon. The spleen may be large and soft. 
No constant characteristic changes have been discovered, either in the 
blood-vessels or the blood, which would satisfactorily account for the ex- 
travasations and other lesioiis. 

The body is apt to decompose early. The skin may be mottled with 
small and large purj)le, blue, brown, or blackish spots produced by de- 
generative changes in the extravasated blood in the cutis. Sometimes 
ulcers are produced by the perforation of effused blood on to the surface. 
The joints may be inflamed, may contain serum or blood. Earely the 
haemorrhages are followed by destruction of the cartilages and ends of 
the bones. Very rarely there is haemorrhage between the periosteum 
and bone, and in the bone itself, iDroducing softening and destruction of 
the bone, and separation of the epiphyses. The sternal ends of the ribs 
are the most frequent seat of this change. Albuminous degeneration of 
the heart, liver, or kidneys, and enlargement of the spleen, are common. 

Infantile Scorbutus. — Infants (under two years) may develop similar 
anaemia and tendency to haemorrhages. The most common location of 
the haemorrhages is beneath the periosteum of the bones of the lower 
extremities, especially of the femora, with separation of the lower epiphy- 
ses. There may be haemorrhages in the skin and subcutaneous tissues, 
the eyelids, and orbit, and in the internal organs. Haemorrhagic inflam- 
mation and ulceration of the gums are usually limited to infants having 
teeth and to portions of the jaAV in which teeth are apparent or just 
about to come into view. ' 

That some forms or phases of scorbutus are of infectious nature is 
not improbable, but definite data in this direction are wanting. 

ACROMEGALIA. 

This rare disease is especially marked by an overgrowth of the ter- 
minal portions of the extremities and of the bones of the face.^ But 

'For a study of scorbutus in infants, "Barlow's Disease," consult Nortlirup and 
CrandalL Kew York Med. .Jour. , May 26tli, 1894. 

See also The American Pediatric Society's Collective Investigation on Infantile 
Scurvy in North America, Transactions of Amer. Ped. Soc, vol. x., 1898, p. 5. 

For a study of histological changes consult Jacohsthal, Ziegler's Beitr. z. path. 
Anat., Bd. xxvii., p. 173, 1900. 

2 Several cases have been described in which there was enlargement of the hands 



GENERAL DISEASES. 337 

there may be a general iuvolvemeut of the skeleton. This excessive 
growth is in the diameter rather than in the length of the bones, and is 
accompanied by local exostoses. Equally important and common is a 
general hyperplasia of the connective tissue of the body. Various lesions 
of the thyroid have been described, but they are not constant. The thy- 
mus may be persistent ; there may be fibrous -tissue formation in the walls 
of the vessels and in the sjmipathetic ganglia. The skin is often i^ig- 
mented. Many visceral lesions have been described. The most con- 
stant lesion which appears to bear upon the etiology of acromegalia is 
that of the pituitary. This in many cases has been found to be the seat 
of lesions, most frequently an hyi^erplasia or adenomatous growth in the 
prehypophysis. ^Tiile sarcoma of the pituitary has been described in 
acromegaly, it seems not unlikely that hyperplasia has, in most cases at 
least, been mistaken for this tumor. It is believed that the hyperplastic 
hypophysis is in some way concerned in inducing the nutritional abnor- 
malities' leading to the general overgrowth of connective tissue and 
bone.^ 

PURPURA. (Purpura Haemorrhagica.) 

This name is applied to a variety of conditions in which extravasa- 
tions of blood are present in the skin or the mucous and serous mem- 
branes. 

Haemorrhages, particularly from the mucous membranes, may be 
severe and even fatal. This condition is often called purpura hsemor- 
rhagica. 

The ecchymoses characteristic of purpura may occur as a result of 
poisoning with certain drugs, and with snake venom ; in various cachectic 
conditions ; in diseases of the nervous system ; in rheumatism ; in gastro- 
intestinal disorders, especially of children. The local ecchymoses in 
pysemia are sometimes classed as a form of purpura, and in these bac- 
teria, especially the ]3yogenic forms, may be demonstrable.^ 



LYMPHATIC CONSTITUTION. (Constitutio Lymphatica ; Status 

Lymphaticus.) 

Attention has been recently called to a series of cases, especially in 
the young and in connection with sudden death, in which there was gen- 
eral hyperplasia of the lymph-nodes, spleen, and thymus, with hypo- 
plasia of the heart and aorta, and often with rickets. 

and feet and lower ends of the long bones, without involvement of the bones of the 
face. "While this condition may follow syphilitic infection, its frequent association with 
pulmonary lesions has led to the designation hype rtropMc pulmonary arthro'patliy . 

^ Successful extirpation of the hypophysis in animals by Friedemann and Maas, re- 
cently made, did not lead to acromegaly. See Berliner klin. Wochenschr. , December 
24th, 1900. 

^ For an excellent resume of acromegalia, with cases and bibliography, see Brooks, 
"Archives of Neurology and Psychopathology, vol. i., p. 485, 1898. 

^For a more detailed consideration in the light of recent studies of cases often 
grouped under the name "Hasmorrhagic Infections," consult Honl, Lubarsch and Oster- 
tag's "Ergebnisse der allg. Aetiologie," Jahrg. i., Ab. 1, p. 793, bibliography. 
22 



338 GENERAL DISEASES. 

Hypoplasia of the heart and aorta is apparently a congenital defect, and 
while not limited to well-defined cases of lymphatic constitution, appears 
in this connection and when occurring alone to mark a noteworthy lack 
of resistance on the part of the organism to various forms of injury, in- 
fection, etc. 

Lymph- Nodes ayid Nodules. — The pharyngeal, thoracic, and abdominal 
lymph-nodes are most frequently involved in hyperplasia, the new cells 
often infiltrating the surrounding tissue. There may be hyperplasia of 
the tonsils, of the cervical, mediastinal, axillary, and abdominal lymph- 
nodes, as well as of the lymphatic tissue of the gastro -intestinal canal. 

The thymus may be congested and large and soft from hyperplasia. 
It sometimes evidently exerts such pressure on the adjacent bronchi and 
large vessels as to lead to death. 

The spleen may be moderately enlarged from hyperplasia, especially 
of the lymphoid tissue of the Malpighian bodies, and it may be con- 
gested.^ 

^ For a study of the lymphatic constitution and its relationship to sudden death, see 
Ewing, New York Med. Jour. , July 10th, 1897, bibliography. 



PART III. 

SPECIAL PATHOLOGY. 



SPECIAL PATHOLOGY. 

General Considerations. 

We have now completed the study of those fundamental processes 
and structural alterations which are embraced in general pathology. 
These have been considered without reference to special regions or organs 
of the body. We now enter upon the study of these pathological proc- 
esses and their associated lesions as they are modified by the special con- 
ditions and characteristic structure of one and another of the tissues or 
organs or regions of the body. It is clear that both the disease processes 
and the structural alterations with which these are associated may be 
modified by the functional and structural peculiarities of the affected 
organ. Thus while degeneration, regeneration, inflammation, etc. , may 
be fundamentally similar, for example, in liver, kidney, and nerve, they 
may i^resent sufficient variation in one or another of these parts to re- 
quire a separate consideration and even a special nomenclature. We 
shall have occasion to call attention now and then to those functional 
and structural characteristics of the organs which often throw much light 
upon their mode of response to the various excitants of disease. 

It is well, on the other hand, to remember that there are in all the 
organs and in most parts of the body certain elementary structures, such, 
as connective tissue, blood- and lymph-vessels, and nerves, whose lesions 
are quite similar wherever they may be. So that many forms of lesion 
involving these structures, while of varying significance to the organism, 
differ in the various parts of the body chiefly in distribution or topo- 
graphy. 



CHAPTER I. 

THE BLOOD ^ AND THE BLOOD-FORMING ORGANS. 

Changes in the Composition and Structure of 
the Blood. 

The Coagulability of the Blood and the characters of the resulting clot 
vary widely, depending partly nx)on the composition of the blood and 
partly upon the conditions under which the coagulation occurs. There 
may be very little coagulation of the blood in death from the exclusion 
of air from the lungs, or from diseases and accidents which interfere 
with the aeration of the blood and permit the accumulation of carbonic 
acid within it. Thus, in death from strangulation or drowning, many 
chronic diseases, scurvy, and under many conditions which we do not 
understand, the blood may remain fluid, or nearly so, after death. On 
the other hand, in a variety of infectious diseases, such as rheumatism, 
pneumonia, etc., very voluminous clots may be formed, although this is 
by no means constantly the case. The fact that large clots form after 
death is not conclusive evidence that an undue amount of fibrin-forming 
elements were present in the blood, nor does the absence of marked coag- 
ulation prove a diminution in the blood of fibrin-forming elements. 

The composition of the clot varies with the rapidity of its formation 
and with the specific gravity of the plasma. Clots very rapidly formed 
in plasma of high specific gravity, or in still slowly circulating blood, 
are apt to be dark red, from admixture of red cells and fibrin. After 
complete failure of circulation, especially in plasma of low specific grav- 
ity, the red cells tend to settle to dependent vessels. Yellowish -white 
succulent clots then form in the clear supernatant plasma, while soft 
black clots result from the excess of red cells collected in the dependent 
vessels. 

The Alkalinity of the Blood, — This varies in health and to a greater 
extent in disease, this variation being parallel with the fluctuations in 
concentration and albumen content. Diminution in the alkalinity of the 
blood is seen in severe anaemia and in diabetes. Increase has been noted 
in catarrhal jaundice. In fever the variations are marked ; they may 
be above or below normal, but a constant change has not been observed. 

Ahhydrsemia — the condition in which the blood contains an excessive 
proportion of albumen, cells, and other solid elements — occurs in dis- 
eases associated with excessive serous discharges from the intestines. It 
is extreme in some cases of cholera, and has been noted in a lesser degree 
in other infectious diseases, as pneumonia and diphtheria. 

' A full discussion of the subjects in this chapter can be found in Ewitig, "Clinical 
Pathology of the Blood," 1901. 



THE BLOOD AND THE BLOOD-FORMING ORGANS. 343 

Hydrsemia is that condition in which the blood contains a large amount 
of water in proportion to the solid ingredients. It occurs in a variety 
of diseases of the heart, lungs, liver, and kidneys, and characterizes all 
forms of anaemia. 

Haemoglobinsemia. — Owing to the destruction of red blood cells in some 
forms of i)oisoning, burning, etc., the blood plasma may contain free 
haemoglobin, by which it is discolored {hcemogloMnwmia) , or it may be 
stained from the absorption of bile x^igment. 

The blood may be actually increased in volume (plethora), either by 
an increase in fluids or in cells, or by simultaneous and proportionate 
increase of both fluid and cellular elements. 

Anaemia. — In general, anaemia means a diminished quantity of blood 
or of red blood cells in the vessels of the whole or any x>art of the body. 
With one exception — mild chlorosis — it is invariably characterized by a 
reduction in number and change in form of the red cells (oligocythaemia), 
and by diminished alkalinity and coagulability. It is always associated 
with a reduction in specific gravity, haemoglobin, and in solid elements. 
Hydraemia and an increased tendency toward osmosis are equally con- 
stant features of this condition. The albumens remaining in the serum 
after coagulation are very slightly diminished in anaemia. 

Generally speaking, anaemia is produced by excessive haematolysis, 
or by defective haematogenesis, or by actual loss of blood, in bulk (haem- 
orrhage), or in its fluid ingredients (transudation). 

Anaemia may be secondary to haemorrhage, to exudative processes, to 
prolonged malnutrition, to chronic organic diseases of many kinds, to 
the action of i^oisons, to congenital hypoplasia of heart and arteries, to 
functional disturbances of an unknown nature in the blood-forming 
organs, and to wholly unknown causes. Simx^le atrophic changes in 
many tissues, hypertrophy of the red marrow, lymiDh-nodes, spleen, liver, 
and thymus, fatty degeneration of the liver, kidneys, heart, and blood- 
vessels, with capillary haemorrhages and transudations, are frequent ac- 
companiments of severe anaemia. 

ALTERATIONS IN THE RED BLOOD CELLS. 

These may be diminished in number and may undergo various 
changes in shape and size and structure. 

Alteration in Number of the Bed Blood Cells. 

Oligocythsemia is that condition of the blood in which the number of 
the red cells is reduced. This reduction in number may be temporary, 
as after haemorrhage, or it may be persistent, as in some forms of anae- 
mia. The number of red blood cells may in extreme cases of anaemia be 
reduced to one-tenth of the normal, or even less ; that is, from the nor- 
mal number, which is between four and five million, there may be a re- 
duction to half a million or less. 



344 THE BLOOD AND THE BLOOD-FOEMIXG ORGANS. 

A persistent diminution in the number of red cells may be effected 
either by increased destruction {luematolysis) or by defective formation 
Quematogenesis) of these elements, but the relation of the two factors in 
the iDroduction of the chronic anaemias is as yet imperfectly determined. 

Excessive h^ematolysis is observed after burns, is produced by 
many mineral poisons, as arsenic, phosphorus, and potassium chlorate, 
in phenylhydrazin poisoning, and may occur in infectious diseases 
through the action of bacterial toxins. All stages of a peculiar de- 
struction of red blood cells may readily be followed in the blood in 
malaria. In chronic infectious diseases, prolonged suppuration, and in 
the cachexia attending malignant new growths, destruction of red cells 
is probably effected, in part, by toxic agents circulating in the blood. 
In pernicious anaemia the condition of the blood may, with considerable 
certainty, be referred largely to a destruction of red cells by some un- 
identified toxic material in the blood. , 

In the process of destruction of the red cells, especially if rapid, 
haemoglobin may be separated from the cells, dissolved in the plasma 
(hsemoglobinaemia), and may then be excreted unchanged in the urine 
( h semoglobinuria) . 

The gradual and more common form of destruction of red cells is 
attended with an alteration of the haemoglobin, effected chiefly in the 
liA^er, and with its deposit in the endothelial and glandular cells of vari- 
ous organs, especially in the liver, sj)leen, kiduej^s, bone marrow, and 
secondarily in any of the tissues. 

A part of the altered haemoglobin is to be found in the form of pig- 
ment granules, or as a diffuse deposit, in the cells of the above-named 
organs, where its content of iron may or may not be demonstrable by 
microchemical tests (hcemosiderin) . Another product of the haemoglo- 
bin, not containing iron, may be found in the same situations, in the 
forms of granules or crystals (Juematoidin). Finally, the derivatives of 
haemoglobin are excreted largely in the form of normal or pathological 
urinary pigment. The remaining fragments and stroma of the red cells 
are soon removed from the circulation largely by leucocytes, and partly 
by endothelial cells and giant cells, in the liver, spleen, and marrow. 

Defective h^matogenesis must be regarded as a cause of such an- 
aemias as are associated w ith pathological changes in the bone marrow 
(pernicious anaemia), and in the lymph-nodes, spleen, and liver (leukae- 
mia). This too is probably the chief cause of the anaemia following 
prolonged malnutrition (secondary anaemia). The pathological changes 
in the blood-producing organs may sometimes arise as primary diseases 
of these organs, or similar changes may be secondary to excessive de- 
mands for the regeneration of the blood. In mild grades of anaemia the 
regeneration of the blood is attended with an hyperplasia of the red 
marrow [containing nucleated red cells of normal size (nonnohlasts)^, 
which replaces the yellow marrow of the long bones. The chief defect 
in the production of red cells may then be a deficiency in haemoglobin 
(chlorosis). In severe and prolonged anaemia, under the influence of 



THE BLOOD AND THE BLOOD-FORMING ORGANS. 345 

toxic agents in the blood, the reproduction of cells may be insufficient, 
and these new cells may be more susceptible to the action of the toxic 
agent, which is itself the cause of their structural defects. A ''circulus 
vitiosus ^' is thus established, the normal development of red cells fails 
and is in part replaced by an abnormal type of blood formation closely 
resembling the embryonal type. In such cases the normoblasts of the 
marrow are replaced by very large nucleated red cells {megcdoUasts) ; 
from these are developed very large red cells which are comparatively 
incapable of the functions of the normal cell. In this way may be es- 
tablished a secondary anaemia which steadily progresses and becomes a 
self-perpetuating disease entirely disproportionate to the original cause 
(secondary pernicious anaemia). 

Alterations in Morphology of the Eed Blood Cells. 

In mild forms of ancemia, the red cells are deficient in hgemoglobin, the 
blood may be pale or watery in appearance, and the cells appear in the 
fresh condition as very pale discs or as slightly refractive rings enclosing 
a nearly colorless central mass. In dry preparations stained with eosin, 
such cells may show only a narrow red ring surrounding a central por- 
tion which is entirely devoid of hgemoglobin. In this grade of anaemia 
there may be noted moderate differences in size and irregularities in 
shape of the red cells. In severe anaemia, under a variety of conditions, 
as after certain forms of poisoning, extensive burns, etc., varying num- 
bers of very small red cells are seen, called microciftes. They are sphe- 
roidal or irregular in shape, may be excessively minute, and their haemo- 
globin is either increased, normal, or diminished. Under similar 
conditions, a variety of bizarre forms of red cells are found, called poilci- 
locytes. In very severe anaemia x^rj large red cells occur in considerable 
numbers. These cells, called megaJocytes, are derived from the large 
nucleated red cells of the marrow, and their appearance in the blood in- 
dicates the early onset or actual establishment of some form of progres- 
sive anaemia (see Plate II., Fig. ii. ). 

Amoeboid movement of megalocytes has been observed in specimens 
examined on a warm stage from the blood of pernicious anaemia. The 
tendency of the red cells to form rouleaux is much diminished or absent 
in very grave anaemia. 

Xot infrequently a loss of haemoglobin is associated with a change in 
the stroma of the cell, so that the mass stains slightly with methylene 
blue. To this change the name of anaemic or polychromatophilic degen- 
eration has been given, and it is thought to show a more or less com- 
plete coagulation necrosis by which change the protoplasm of the red cell 
becomes more basophilic' in its staining reaction. Instead of a uniform 
loss of haemoglobin this constituent of the cell may be condensed in the 

^ It is convenient to classify the dyes used in staining into the acid, the neutral, and 
the basic, and to designate cells, in accordance with the relative persistency with which 
they hold these dyes, as neutrophile, acidophile, or basophile. 



Desckiption of Plate II. 

Fig. I. Normal Blood. — Ehrlicli's triacid stain. The red cells are of nearly uni- 
form size and shape. There is an abundance of haemoglobin which is evenly distrib- 
uted, but less densely at the centre of the cells, except in those cells which have been 
very rapidly dried, when the central lighter area does not appear. On the left is a 
lymphocyte without visible protoplasm. Above and below are two mononuclear cells 
showing varieties in the staining quality of the nucleus. In the centre is a large mono- 
nuclear or transitional leucocyte. The fine neutropliile granules and the large eosino- 
phile granules are nearly identical in color and are to be distinguished, with this stain, 
only by difference in size. 

Fig. II. Chlorosis.— M. M., female, 28 years. Red cells, 3,400,000. Hb., thirty - 
five per cent. Eosin and methylene blue. The red cells are moderately reduced in 
number and there are moderate variations in their size and shape. They show a uni- 
form and nearly invariable diminution in hnemoglobin. In the upper left quadrant is 
a cell showing a gathering of haemoglobin into a dense central mass. In a cell on the 
left is represented the appearance in the central portion of a mass devoid of haemoglobin 
and staining lightly with methylene blue. Such degenerative changes are common in 
anaemic blood and are not to be confounded with nucleated red cells, normoblasts, one of 
which is shown in the upper right quadrant. The polynuclear and large mononuclear 
leucocytes are intended to represent the mixed leucocytosis of this condition. Above 
are a few blood plates. 

Fig. III. Primary Progressive Pernicious Anemia. — O. H., 44 years. Red 
cells, 675,000. Hb. , fifteen per cent. Eosin and methylene blue. The red cells are very 
much reduced in number, and do not form rouleaux. There are extreme variations in 
size, shape, and quantity of haemoglobin. The large nucleated red cells, megalohlasts and 
gigantohlasts, were rather numerous. The upper one shows a small nucleus in the rest- 
ing stage, the lower one a nucleus in early mitosis. The megalocyte in the centre shows 
an excess of haemoglobin, the one at the base of the field is deficient in haemoglobin and 
its outline is imperfect. In this case the eosinopliile cells and the mononuclear leuco- 
C3^tes were increased in number. 

Fig. IV. Secondary Pernicious Anemia. — C. N., 29 years. Chronic malaria. 
Red cells, 1,900,000. Hb., twenty -five per cent. Triacid stain. The red cells show 
extreme differences in size, shape, and content of haemoglobin. Most of the cells are 
deficient in haemoglobin. Nucleated red cells were not seen. The leucocytes, espe- 
cially the polynuclear forms, were increased in n\imber, and a few myelocytes were pres- 
ent, one of which is shown on the right. 

Fig. Y. Ly]mphatic Leukemia. — Eosin and methylene blue. The red cells are 
much reduced in number but do not show great differences in size, shape, or content 
of haemoglobin. No nucleated red cells were found. The increased number of leuco- 
cytes consisted principally of small and large mononuclear cells. On the left is seen 
a basket-shaped nucleus without demonstrable cell body. 

Fig. VI. Myelogenous Leukemia. — Triacid stain. The red cells are much re- 
duced in number, show moderate differences in size and shape, but usually contain an 
abundance of haemoglobin. A few normoblasts were seen. The increased number of 
leucocytes consists largely of myelocytes and polynuclear leucocytes. In the centre is a 
large myelocyte with very pale eccentric nucleus. Above are myelocytes of ordinary 
size and with more deeply staining nuclei. On the right is a large eosinophile myelocyte. 



Pathological Anatomy and Histology. 
Delafieid and Prudden. 



Plate 11 



^ 



• 









«f 



PIG. I. NORMAL BLOOD, 

(Bhrlieii's Triaeid Stain.) 



FIG. n. CHLOROSIS. 

(Sosin and Methylene Blue.) 






m 






\ 







i0^-^. 



.^mi^. 



ii ^# 



PIG. m. PRIMARY PERNICIOFS AN^SIMIA. 
(Eosin and Methylene Blue.) 



PIG. IV. SECONDARY PERNICIOITS AN 
(Ehrlich's Triaeid Stain.) 




PIG. V. LTENO-LYMPHATIC LBITK^EJMIA. 
(Eosin and Methylene Blue.) 



/ 






-5^i!fc 



''^M 



..vvg»v:. 'W;y 






^P^.fi 



5»- V 



y^^^ 



PIG. VI. MYBLOGENOTTS LEUKiRMI A —NEARLY 

PURE TYPE. 

(Ehrlich's Triaeid Stain.) 



CHANGES IN THE STRUCTURE OF THE BLOOD. 



DRAWN BY JAMES EWING. 



THE BLOOD AND THE BLOOD-FORMING ORGANS. 347 

form of small granules occupying the cell body and staining more deeply 
with methylene blue than do normal cells (granular degeneration). 

It should be remembered that during the manipulations recxuired in 
making dried specimens the red cells may suffer a variety of artificial 
changes, many of which are very confusing. 

Nucleated red blood cells are found in the blood in all forms of anaemia, 
and their ai^pearance indicates regenerative activity on the part of the 
blood-producing organs. Their presence in the blood, though at all 
periods of extra-uterine life abnormal, may usually be regarded as of 
favorable import in disease. Within a few hours after severe haemor- 
rhage nucleated red cells may be noted in considerable numbers. ' Dur- 
ing the regeneration of the blood in anaemia, the occurrence of nucleated 
red cells is nearly constant, btit subject to rather sudden iDcriodical A'ari- 
ations sometimes called ^' blood crises.'^ In favorable cases of anaemia 
nucleated red cells of normal size only (normoblasts) Plate II., Fig. 
ii. ) are to be seen, whose compact, darkly staining nucleus may be found 
either in the centre of the cell or slightly protruding from the periphery ; 
or, nuclei apparently quite extruded from the cell may be found free in 
the plasma. 

In severe anaemia attended with an abnormal tyj)eof blood formation, 
very large nucleated red cells {megaloblasts) (Plate II., Fig. iii.) appear 
in varying numbers. The j)rotox)lasm of these cells often shows an ex- 
cess of haemoglobin, but frequently the reddish-brown stain produced by 
eosin indicates an altered form of haemoglobin, or very fine basophile 
granules may be demonstrated by treatment with methylene blue. The 
nuclei of the megaloblasts may be single and compact, or a single large 
nucleus may show stages of direct division, or in extremely large cells 
{gigantoblasts) (Plate IL, Fig. iii.) the nuclei may present phases of nor- 
mal or pathological mitosis. 

ALTERATIONS IN THE WHITE BLOOD CELLSo 

The Leucocytes of Normal Blood. 

The leucocytes of normal blood may be classified according to their 
place of origin, or by the character of their nuclei, or by the reac- 
tion of the granules in their protoplasm to certain dyes. The most ser- 
viceable classification is that based both upon the character of the nucleus 
and upon the reaction of the protoplasm to dyes, according to Avhich we 
may distinguish in normal blood the following forms (see Plate II. , 
Fig. i.): 

1. Lymphocytes, small leucocytes of about the size of red cells or 
larger, with a single com]3act, deeply staining nucleus, surrounded \)\ a 

' The appearance of nucleated red cells and abnormal forms has been frequently 
noted in those who have recently arrived in mountainous regions, the probable explana- 
tion being that the lowered oxygen tension of the rarefied air demands a larger amount 
of haemoglobin to supply the wants of the tissues, with the result that for a short time 
immature red cells are set free from the bone marrow. 



348 THE BLOOD AND THE BLOOD-FOEMINGr ORGANS. 

thin rim of homogeneous protoplasm. The cell body usually possesses a 
stronger basophilic reaction than the nucleus, so that in staining with 
methylene blue the nucleus shows as a pale spot in the centre of the dark 
ring of the cell body. This ring is often ragged in its outline and may 
show distinct projections which are sometimes cast off into the circulating 
blood. Large and small lymphocytes may be distinguished (Plate II., 
Fig. v.). 

2. Large Mononuclear Leltcoca^tes, with a single, compact or 
vesicular, rather faintly staining nucleus and a relatively large amount 
of protoplasm which stains much less strongly than the nucleus, thus 
separating this group from the lymphocytes. 

3. Transitional Leucocytes, of the same size as many of the large 
mononuclear leucocytes, with a compact or vesicular, irregular or in- 
curved nucleus, and a considerable mass of protoplasm, in which fine 
neutrophile granules can occasionally be demonstrated. 

4. Polynuclear I^eutrophile Leucocytes, of the same size as 
the transitional leucocytes, with a i)artially or completely divided nu- 
cleus, of which the separate portions are either compact or vesicular, 
deeply or faintly staining, and with considerable protoplasm in which 
distinct granules may be demonstrated by the neutral dyes. 

5. EosiNOPHiLE Cells, of the same characters as the ordinary poly- 
nuclear leucocytes, but containing in their bodies large refractive gran- 
ules which stain deeply with so-called acid dyes such as eosin. 

6. Mast Cells, of about the same size as the polynuclear cells, but 
containing coarse granulations stained only by basic dyes such as meth- 
ylene blue. The nucleus is small, stains feebly, and is usually lobular. 
It is often covered very largely by the granulations. 

These various forms of leucocytes occur in normal blood in the fol- 
lowing proportions, which represent averages only and are subject to 
considerable variations: 

Polynuclear neutrophile leucocytes 70 to 72 per cent. 

Large mononuclear and transition forms 2 " 4 " 

Lymphocytes 22 " 25 " 

Eosinophiles 2 " 4 " 

Mast cells less than 0. 5 " 

In the normal blood of young children the relative proportion of 
mononuclear cells is considerably greater than in that of adults. 

The numbers and i)roportions of the polynuclear leucocytes are in 
disease subject to very wide variations, and some abnormal forms of 
colorless cells make their appearance in the blood. 

Leucocytosis. 

Leucocytosis is that condition of the blood in which the leucocytes 
are temporarily or persistently increased in number. When several 
forms of leucocytes are increased in number and the usual proportions 
are but partially disturbed, we speak of mixed leucocytosis. Such a con- 



THE BLOOD AND THE BLOOD-FOEMING OEGANS. 349 

dition is seen in some forms of anaemia. \Ylien the polynnclear neutro- 
phile leucocytes alone are increased the condition is termed polynuclear 
leucocytosis, or simply leucocytosis. If the mononuclear cells are chiefly 
affected, the condition maybe denoted as lymplwcytosis. The eosinoj)hile 
cells alone may be increased. 

Polynudear Leucocytosis may be either physiological or pathological. 

Physiological Polynudear Leucocytosis is seen during normal digestion, 
in the later months of pregnancy, in the first days of infancy, and is 
usually of moderate grade. 

Pathological Polynudear Leucocytosis occurs in many inflammatory and 
infectious diseases, and accompanies the various cachexias. Of the in- 
fectious diseases attended with leucocytosis may be mentioned pneu- 
monia, diphtheria, scarlet fever, erysipelas, rheumatism, suppuratiye 
cerebro- spinal meningitis, and any disease associated with a pronounced 
exudative or suppurative lesion. On the other hand, leucocytosis is 
absent in uncomplicated typhoid fever, typhus, malaria, measles, and 
tuberculosis. 

The origin and significance of the leucocytosis of infectious diseases 
is imperfectly understood, but may be partially exjDlained by the princi- 
ples of chemotaxis and phagocytosis. From exj)erimental evidence and 
clinical observation it is known that during the onset of some infectious 
diseases the entrance of bacteria or their products into the blood is fol- 
lowed by a disapiiearance from the circulation of many polynudear leu- 
cocytes, which are removed from the larger vessels and lodged in the 
capillaries, princiiDally in the lungs and liver. This condition of the 
blood, called hypoleucocyiosis, may be attended with a transient reduction 
in temperature and weakening of the heart's action, and is usually suc- 
ceeded shortly by the reappearance of polynudear leucocytes in large 
numbers, and by a rise of temperature. These leucocytes are apt to 
gather in regions in which micro-organisms are abundant, and are be- 
lieved to take nj) and destroy micro-organisms (phagocytosis), and to 
prevent their further entrance, and possibly the entrance of their prod- 
ucts also into the circulation. Of the place and method of origin of 
these new leucocytes very little is definitely known. 

In many very severe cases of infectious disease, such as pneumonia, 
diiDhtheria, and peritonitis, the initial hypolencocytosis persists, in which 
event the disease usually runs an asthenic and fatal course, with a ten- 
dency to low temperature and feeble pulse. 

A^Hien leucocytosis is established the grade varies frequently with the 
extent of the local lesion and the height of the fever associated with 
the infectious process, and disappears with, or soon after, the decline of the 
disease. In general, according to our present knowledge, the leucocy- 
tosis of infectious diseases may be regarded as the effort of the blood - 
producing organs to protect the blood and tissues by means of leucocytes 
against the invasion of micro-organisms and against the action of toxins 
present in the circulation. 

The blood in typhoid fever presents a peculiar variation from that in 



350 THE BLOOD AND THE BLOOD-FORMING ORGANS. 

most infections diseases. In the first weeks of the disease there is usu- 
ally a reduction in the number of leucocytes, especially of the polynuclear 
forms. In the later weeks the lymphocytes may form eighty per cent 
of the leucocytes present in the blood. Each relapse is attended with an 
increase of the lymphocytosis, while an increase of polynuclear leucocytes 
usually occurs with complications only. 

In the various forms of tuberculosis there is no leucocytosis unless 
the lesion is markedly exudative in character, or is complicated by sup- 
puration or chronic anaemia. It is especially in pulmonary tuberculosis 
that secondary infection with the pyogenic cocci produces exudative or 
suppurative lesions such as are apt to accompany leucocytosis. 

Cachectic Leucocytosis is a feature of altered conditions of the blood, 
such as are associated with the growth of malignant tumors, and with 
many diseases producing secondary anaemia. This increase of poly- 
nuclear leucocytes may serve to distinguish many forms of secondary 
from primary anaemia. The inflammation and toxaemia accompanying 
many new growths afford a sufficient reason for the appearance of ca- 
chectic leucocytosis, but under many other circumstances its direct cause 
is less apparent. ' 

Hypoleucocytosis occurs not only in infectious diseases, when the poly- 
nuclear cells alone are reduced in numbers, but also from shock, reduc- 
tion of body temperature, and exhaustion, when all forms of leucocytes 
may be diminished. It is a fairly constant feature of i)rimary pernicious 
anaemia.^ 

Polynuclear Eosinophile Leucocytosis is found in a number of unrelated 
conditions. In bronchial asthma the eosinophile cells are considerably 
increased, often forming ten to twenty per cent of the total white cells. 
In acute and chronic diseases of the skin, such as pemphigus, prurigo, 
and psoriasis, the eosinophiles are often increased to a marked degree, 
but the condition is not constant. In trichinosis and helminthiasis the 
increase is so constant that it becomes of diagnostic value in these con- 
ditions. A post-febrile eosinophilia is frequently observed. 

Lymphocytosis, frequently seen in the anaemias and acute intestinal 
disorders of childhood, has also been noted in some forms of secondary 
anaemia (syphilis), and in an extreme degree as the chief characteristic 
of the blood of lymphatic leukaemia. 

In mixed leucocytoses a number of types of cells appear which are de- 
rived from the bone marrow and differ greatly from the forms already 
described. Of these the most important are the myelocytes (Plate II. , Fig. 
vi. ) . These are mononuclear cells with an oval, faintly staining nucleus 
concentrically placed, and the cell body contains a greater or less number 
of neutrophile granulations. They are usually about twice as large as 

' For further data concerning Leucocytosis, consult Rieder, " Beitrage zur Kenntniss 
d. Leukocytose," Leipsic, 1892. Turk,'' Klin. Untersuchungen u. d. Verhalten d. Blutes," 
etc., Wien. 1898. 

'^For Hypoleucocytosis, cons>\x\.i Loicit, "Studien liber Physiol, und Pathol, d. Blutes 
u. d. Lymphe," Jena, 1892. Ewing, "Toxic Hypoleucocytosis," New York Medical 
Journal, March, 1895. 



THE BLOOD AND THE BLOOD-FORMING ORGANS. 351 

the red cells, but may be of practically the same size. Another type pos- 
sesses the same characteristics except that the granulations are of the 
eosiuophile variety. Finally, there are found under the same conditions 
as the myelocytes large mononuclear cells without granulations, the so- 
called 'irritation forms. ^' The nucleus stains deep blue with the triacid 
stain, and the cell body a dark brown. Moderate degrees of mixed leu- 
cocytosis are seen in the severe primary and secondary ansemias, during 
the course and at the end of severe infections, especially in children, 
but the most marked example is in the blood of spleno -myelogenous 
leukgemia. In this disease also, especially in the more chronic forms, the 
mast cells may be very abundant, and show a slightly different type from 
those found in normal blood. They are much larger, often mononuclear, 
and the granules are very irregular in size. 

Charcot- Leyden crystals are occasionally found, chiefly after death, in 
the blood in leukaemia, usually at the same time with an increased num- 
ber of eosiuophile cells. 

Degenerative Changes in the Blood are usually indicated in the leuco- 
cytes by variations in the percentage of normal and abnormal varieties, 
rather than by alterations in the individual cells, for degenerating leuco- 
cytes are usually quickly removed from the circulation. Staining re- 
actions of the various granules, by which degenerative changes may be 
recognized, have not yet been devised. In leuksemia, pernicious anae- 
mia, and diphtheria, a diminished reaction to nuclear dyes has been 
observed. In leukaemia, and in the severe infectious diseases, the leuco- 
cytes may be extremely cohesive, and it is believed that a large quantity 
of bacteria or toxins in the circulation may even effect a complete solu- 
tion and destruction of leucocytes (leucocytolysis). Fatty degeneration 
of leucocytes has been demonstrated. 

Melanaemia. — In this condition the blood contains larger and smaller 
irregular-shaped i^articles or masses of brown or black pigment. This 
condition is most frequently the result of intermittent and remittent 
fever, particularly the severer forms. It may be accompanied by anae- 
mia and leucocytosis. It does not occur in all cases of the above-named 
affections. It may be transient in character. The pigment may be free, 
or more usually is enclosed in leucocytes. Under the same conditions 
l)igment may be deposited in the liver, spleen, lymph-nodes, bone mar- 
row, and blood-vessels. Owing to the deposit of pigment in the organs 
they may assume a gray or slate color. The pigment developed in 
malaria originates in the decomposition of the haemoglobin under the 
influence of the Plasmodium. Pigment which has been taken into the 
lungs from the air, such as coal dust, etc., may find its way into the 
blood either before or after deposition in the bronchial or other lymph - 
nodes, and may be afterward deposited in the spleen and liver. ' 

^ For further details concerning changes in the blood, consult Si?non, " Clinical 
Diagnosis," 3d ed. Ewing, "Clinical Pathology of the Blood," 1901. Cabot, "Clinical 
Examination of the Blood," 



352 THE BLOOD AND THE BLOOD-FORMING ORGANS. 



Methods of Examination of the Blood. 

The blood may be examined fresh on the warm stage without the addition of any- 
fixative, simply surrounding the cover with oil or vaselin to prevent evaporation. 
This method is especially useful in the examination of blood for the plasmodiamalarise. 
For most purposes, however, the cells should be treated the instant the blood leaves 
the vessels in such a way as to retain their normal form. This fixation may be accom- 
plished by the use of chemical agents (wet method) or by quick drying on the cover 
glass or slide (dry method). 

Wet Method. — Among the chemical fixative agents are osmic acid and a solution 
of corrosive sublimate. Osmic acid : A drop or two of blood drawn from the cleansed 
finger-tip by a needle prick is allowed to fall into a cubic centimetre of from one- to 
two-per-cent osmic acid. After an hour the blood cells may be transferred by a pipette 
to a solution of acetate of potash, in which they may be preserved. 

Sublimate may be used in the form of Hayem's solution, consisting of 

Chloride of sodium 1 gm. 

Sulphate " 5 " 

Corrosive sublimate 0.5 " 

Water, distilled 200 

The blood is received directly into this solution, in which it is studied. The wet 
method of fixation is especially to be recommended for studies on the minute structure 
of blood cells. 

Dry Method. — It has been found that if the freshly drawn blood from a finger 
prick be immediately dried on a glass in a very thin layer, the cell forms are quite well 
preserved and may be exposed to the action of staining agents.^ 

For this purpose square cover-glasses of medium size should be cleaned in strong 
nitric acid, rinsed in alcohol and ether, carefully dried, and kept free from dust. A 
drop of blood may be expressed by very light pressure only from the finger tip, previ- 
ously cleansed with alcohol and ether, and for the best results the drop must be spher- 
oidal and about one-sixteenth of an inch in diameter. One cover-glass should be held 
in the forceps, or between the fingers if thoroughly dry, and its central point touched 
to the drop of blood. After contact with the blood this cover-glass should be instantly 
laid upon a second glass so as to cover all but an eighth of an inch along one side, and 
as soon as the blood has spread to the edges, the cover-glasses should be quickly sepa- 
rated by sliding without pressure and dried in the air. If, instead of drying in the air, 
the specimens are rapidly dried high over an alcohol flame, the fixation will be more 
successful, and many artificial changes in the red cells will be avoided. 

Another method, more successful in many hands, consists in touching the drop 
with the smooth edge of a glass slide, applying this edge with its adherent blood 
obliciuely to a slide, and when the blood has spread along the edge of the slide, drawing 
it rapidly across the surface of the second slide. 

For the permanent fixation of the cells and to prevent their solution by strong dyes, 
one of two methods may be recommended, with preference in the order named : 

1. Ehrlielis Method. — The specimens are heated in a hot-air bath or on a copper 
plate, for from five minutes to two hours at a temperature of 110° C. to 120° C. 

2. JSikiforoff's Metliod. — The specimens are placed for half an hour in equal parts 
of alcohol and ether. 

Various staining agents are to be employed according to the object in view. Prob- 
ably most information is gained from specimens stained by the triacid mixture of Ehr- 
lich, Avhich is thus prepared ^ : 

' Oraicitz, "Methodik der klinischen Blut-Untersuchungen," Berlin, 1899. Ehrlicli 
and Lazarus, "Die Anoemie," Wien, 1898. 

■^ Great care must be used in selecting these dyes. Those made by Griibler, of Leip- 
sic, are reliable. It is far better to purchase the solution already mixed as sold by 
Grubler under the name of "triacid mixture for neutrophile granules." 



THE BLOOD AND THE BLOOD -FORMING ORGANS. 353 

Saturated aqueous solutions of 

Orange G 13 to 14 o.c. 

Acid f uchsin 6 " 7 " 

Methyl green 12.5 " 

To the mixture of these add 

Water 15 c.c. 

Absolute alcohol 25 " 

Glycerin 10 " 

The specimen should be stained in this fluid for three to five minutes, washed in 
water, dried, and mounted in dammar dissolved in xylol. 

The red cells are then found stained orange-yellow, the nuclei dark-green or blue, 
the neutrophile and eosinophile granules dark-red. The mast-cell granules are not 
stained. 

Rather more uniform results, especially as regards the red cells, may be obtained by 
the following method, which also demonstrates the malarial Plasmodium and basophile 
granules, but not the neutrophile granules: Place the specimens for two minutes in a 
saturated alcoholic solution of eosin, wash in water, and counterstain for five minutes 
in a one-per-cent watery solution of methylene blue. The red cells and eosinophile 
granules then appear bright-red. The nuclei, basophile granules, and malarial Plasmo- 
dia are stained blue. 

Recently a stain has been devised by Jenner^ which bids fair to supplant other 
methods on account of its simplicity, rapidity, and ease of application. It consists of a 
half-per-cent solution in methyl alcohol of a compound made by mixing a 1.2 per cent 
aqueous eosin and a one-per-cent aqueous methylene-blue solution. The precipitate 
which forms is filtered off, dried, and dissolved in the methyl alcohol. The blood smears 
are fixed by this solution in from one to three minutes. The red cells are of a terra cotta 
color, the nuclei blue, the neutrophile and eosinophile granules red, the mast-cell gran- 
ules purple; bacteria, malarial organisms, and blood plaques blue. 

For the demonstration of /«^ in blood from a finger prick, cover-glass preparations 
dried in the air should be stained for twenty-four hours in one-per-cent aqueous solution 
of osmic acid. To avoid numerous sources of error, a control preparation should be 
previously placed in chloroform for twenty -four hours to dissolve the fat, and the two 
specimens carried together through the osmic acid. In the one, black fat droplets will 
be seen, which should be entirely absent in the other. 



FOREIGN BODIES IN THE BLOOD. 

Various bodies which do not belong there, aside from those above 
mentioned, may find access to the vessels and mingle with the blood. 
Pus cells may get into the blood from the opening of an abscess into a 
vessel or from some inflammatory change in its walls. Desquamated 
endothelial cells from the vessel walls, either in a condition of fatty de- 
generation or in various stages of proliferation, may be mingled with the 
normal blood elements ; also tumor cells of various kinds, fragments of 
disintegrated thrombi, portions of heart valves, etc. Crystals of bili- 
rubin have been found in the blood in icterus. 

Fat, in a moderate amount, is a normal ingredient of the blood during 
digestion and in lactation. Under pathological conditions it may occur 
in larger and smaller droplets. This lijmmia occurs as a result of deficient 
oxidation, in diabetes, in drunkards, and in some cases of dyspnoea from 
various causes. The droplets are small and liable to escape observatiouc 

^L. Jeiiner, Lancet, 1899, vol. i., p. 370. 
23 



354 THE BLOOD AND THE BLOOD-FORMING ORGANS. 

lu many cases of injury, particularly in crushing fractures of the 
bone, the fat of the marrow finds its way into the blood, and it may col- 
lect in large droits in the vessels of the lungs, forming the so-called /rt^ 
emboli (Fig. 13, p. 75) ; or it may pass the lungs and form emboli in 
other parts, as the brain, kidneys, etc. Fat embolism in eclampsia is of 
occasional occurrence. 

The fat may be absorbed from the vessels, having produced little or 
no disturbance ; or in some cases it may produce serious results by the 
stoppage of a large series of vessels in the lungs, brain, or other parts of 
the body.' 

Tissues and organs whose blood-vessels are suspected to contain fat droplets should 
be fixed with osmic acid, which stains fat black. Sections without further staining 
may be mounted in glycerin. 

Air, as a result of an opening in the veins, is of occasional occurrence. 
If the amount of air be small, it appears to be readily absorbed, and does 
little or no harm. If, on the other hand, a large quantity is admitted to 
the veins at once, it collects in the right side of the heart, from which 
the contractions of the organ are unable to force it in any considerable 
quantity, and, the supply of blood being thus cut off from the lungs, 
death very quickly ensues. The blocking of the smaller pulmonary ves- 
sels and of the vessels of the heart with air bubbles may also hasten 
death. It is especially from wounds of the veins of the neck and thorax 
that the accident is most apt to occur. But it may be due to the intro- 
duction of air into the uterine veins in intra-uterine injection, or in the 
removal of tumors.^ One should remember in this connection that in- 
fection with bacillus aerogenes gives rise to gas bubbles in the blood-ves- 
sels, as well as in other tissues (see page 243). 

Parasites and Other Foreign Bodies in the Blood. — The occurrence of 
animal and vegetable parasites is considered more in detail in parts of 
this book devoted to these organisms. It will suffice to mention here 
that the more important of the animal parasites of the blood are: The 
Filaria sanguinis hominis, the Distoma hcematoMum, and the embryos of 
trichina and echinococcus, which are of occasional and usually temporary 
occurrence. 

The various forms of bacteria which may be found in the blood will 
be considered in parts of this book in which these organisms are treated 
in detail.^ Parenchyma-cell emboli are considered on page 75. 

^ For resume of this subject with bibliography, consult Welch in article on Embolism 
in Allbutt's "System of Medicine," vol. vi., p. 258. 

''Welch, ibid., p. 254. 

3 For methods and results of bacterial studies of the blood with bibliography, con- 
sult Kuhnau, Zeit. f. Hygiene, Bd. xxv., p. 492, 1897. 



THE BLOOD AND THE BLOOD-FOEMING OEGAN^S. 355 



General Diseases Involving the Blood and Blood-Forming 

Organs.' 

There is a group of diseases in which the essential lesion seems to be 
an alteration in the composition of the blood, although in some members 
of the group other lesions are also i)resent. This group embraces Chlor- 
osis, Secondary and Pernicious Anaemia, Leukaemia, and Pseudo- 
leukaemia. 

CHLOROSIS. 

Chlorosis is a disease of the blood, attended with a diminution in the 
haemoglobin, and usually in the number of the red blood cells. 

Of the essential element in the incitement of this disease and of the 
exact method of its origin we are ignorant. The condition has been at- 
tributed to congenital hypoplasia of the heart and blood-vessels, to pro- 
longed malnutrition, to intestinal intoxication, and to functional dis- 
turbance of an unknown nature in the blood-producing organs. 

In the mildest grade of chlorosis the only change to be observed is a 
diminution of haemoglobin. In severer forms may be added a diminution 
in number and moderate variations in size and shape of the red cells. In 
very severe and relapsing cases the haemoglobin may be excessively de- 
creased ; the red cells may number less than two million jDcr cubic milli- 
metre, and the average size of the cells be less than normal. The leucocytes 
are not increased in number. There may be a slight relative increase of 
the lymphocytes ; megalocytes, microcytes, and poikilocytes may appear 
(see Plate II., Fig. ii.). 

The specific gravity of the blood is diminished ; the alkalinity of the 
blood and serum is, as a rule, diminished slightly, while the power of 
coagulation remains normal. Even in cases of considerable severity the 
degenerative changes in the viscera characterizing other forms of anaemia 
have been found wanting, although degenerative changes in the red cells 
may occur in accordance with the severity of the disease. The liver does 
not contain an excess of iron, and the urine is free from pathological 
urinary pigments. 

The regeneration of the blood in chlorosis under rest and treatment 
with iron may usually be rather promptly effected by increased activity 
of the red marrow which is probably hyperi^lastic. This regenerative 
process may be indicated in the blood by the periodical appearance of 
considerable numbers of normoblasts. The appearance of these nucleated 
red cells may be accompanied by a moderate increase of leucocytes, both 
mononuclear and polynuclear. Myelocytes also may rarely be seen. 

' For a full discussion of the subjects treated in this chapter the reader is referred 
to Von JSfoorden, "Bleichsucht." Xothnagel's " Spec. Path. u. Therap."; and to Ehrlich 
and Lazarus, "Die Anaemie," Nothnagel's "Spec. Path. u. Therap." 



356 THE BLOOD AND THE BLOOD-FORMING ORGANS. 



SECONDARY ANiEMIA. 

While chlorosis may be considered usually a disease of adolescence, 
and while its occurrence is almost wholly confined to the female sex, 
there is another ty]3e of blood change which seems best classified under 
the heading of secondary ansemia, and which is independent of sex or 
age. The determining agents are either of a general nature, such as poor 
food and bad air, or they are actual diseases, or they may be intestinal 
parasites, or finally chronic poisoning. Among those diseases which are 
likely to induce a well-defined angemia we may mention prolonged sup- 
puration, diseases of the stomach and intestines, malaria, syphilis, and 
malignant tumors. The intestinal i^arasites are chiefly the Aukylostoma 
duodenale and the Bothriocephalus latus. The poisons are lead and, 
more rarely, arsenic. The alterations which are apparent on examining 
the blood are very variable, depending upon the agent. The haemoglobin 
is regularly diminished to a greater per cent than the red cells ; it may 
fall as low as 15-20 per cent ; the red cells rarely fall below one million. 
^N^ucleated red cells of the normoblastic type are frequent in the severe 
cases ; megaloblasts are not found except in the most advanced cases, and 
then in small numbers. As a rule the average diameter of the red cells 
is slightly below normal, with a moderate poikilocytosis. Granular de- 
generation is present to a variable extent in the red cells except in malaria 
and lead poisoning, when it is the rule. In the anaemias produced by 
the intestinal worms the blood j)icture may be that of pernicious anaemia, 
with a great increase in the size of the cells and the apj)earance in the 
blood of numerous megaloblasts, thus forming an exception to the general 
rule that the blood of secondary anaemia is normoblastic in tyi3e. The 
leucocytes are increased, as a rule, in cases due to suppuration and to 
tumors ; in other forms there is usually but little change in the number, 
though it is impossible to formulate a general rule. 



PERNICIOUS ANEMIA. 

Pernicious anaemia is a disease of the blood and blood-forming organs, 
characterized by excessive destruction associated with defective produc- 
tion of red cells. 

The exact relation of the factors concerned in the causation of the 
disease has not been determined. It may be said, however, that while 
very rapid cases of pernicious anaemia have been observed unaccom- 
panied by the usual lesions in the bone marrow associated with defective 
haematogenesis, the disease seems not to exist without excessive haemato- 
lysis. 

Pernicious anaemia may probably originate as a primary disease of 
the blood or bone marrow, but many cases apparently primary have 
been shown at autopsy to be secondary to such conditions as cancer, 
nephritis, tuberculosis, atrophy of the gastric mucosa, or the presence of 



THE BLOOD AND THE BLOOD-FORMIXG ORGANS. 357 

parasites iu tlie blood or intestiue. The studies of HuBter indicate that 
the destruction of the blood may iu some cases result principally iu the 
portal circulation and particularly iu the spleen from the action of toxic 
substances absorbed from the intestines. Whatever its origin, the dis- 
tinguishing feature of i)ernicious ansemia is the fact that the ansemia is 
entirely disproportionate to any apparent cause, and when once estab- 
lished tends to progress to a fatal issue. 

The essential lesion is an extreme and iDrogressive diminution in num- 
ber and very great variation in size and form of the red blood cells (see 
Plate 11. , Figs. iii. and iv. ). Nearly constant is a widely distributed 
lesion of the bone marrow, in which the normal nucleated red cells are 
partly replaced by an excessive number of larger nucleated corpuscles or 
megaloblasts, with atrophy of fat cells. The destruction of hsemoglobin is 
followed by a considerable deposit of iron in the liver, spleen, marrow, 
and other organs, and by the apijearauce of abnormal pigment in the 
urine. The prolonged anaemia may be accompanied by fatty degenera- 
tion in the viscera, especially of the liver, kidneys, and heart muscle. 
As a combined result of fatty changes in the arterial walls and of the 
diminution in albuminous ingredients and in the coagulability of the 
blood, haemorrhages in various j^arts of the body, especially the retina, 
are of frequent occurrence. Disseminated areas of sclerosis in the spinal 
cord have been described and regarded as the result of minute haemor- 
rhages in this region. 

In the blood the red cells are usually reduced to less than two million 
and often to half a million i^er cubic millimetre. Of the remaining cells 
a considerable percentage may be abnormally large (megalocytes), or 
very small (microcytes). Cells of very irregular shape are often present 
in abundance (poikilocytes) (Plate II., Fig. iii.). The quantity of 
haemoglobin iu the majority of the cells is usually increased, but may be 
diminished in a certain proportion of cells, which then resemble those 
found in chlorosis. The '' haemoglobin index" — that is, the relation of 
the total percentage of haemoglobin to the total number of cells — may be 
normal when a deficiency of haemoglobin in one cell is counterbalanced 
by a i3roj)ortionate excess in another. 

A variety of degenerative changes iu the red cells are commonly 
present, including especially those alterations in the staining reactions of 
the protoplasm known as polycliromatopMlia and grcmtdar degeneration. 
In the first the cell stains a more or less uniform blue with methylene 
blue ; in the second the cells contain granules which give a strong baso- 
philic staining reaction. 

Nucleated red cells of normal size (normoblasts) are of frequent oc- 
currence in the blood of well-established pernicious anaemia. Abnormally 
large nucleated red cells (megaloblasts) are a nearly constant element 
and are of great diagnostic imj)ortance, as they indicate the presence of 
a grave lesion in the bone marrow. They are rather more abundant 
than the normoblasts in well -developed cases. 

Megalocytes and megaloblasts usually show an excess of haemoglobin. 



358 THE BLOOD AND THE BLOOD-FORMING ORGANS. 

may exhibit amoeboid movement, and have no tendency toward the 
formation of ronleanx. Extremely large nucleated red cells (giganto- 
blasts) are frecxnently found in advanced cases, and in these cells as well 
as in the megaloblasts the nuclei may be rarely seen in various stages of 
normal or pathological mitosis. '^ Blood crises," by which is indicated 
the appearance of large numbers of normo- or megaloblasts in the circu- 
lation, may occur in pernicious anaemia, but it must be remembered that 
the blood picture in any severe anaemia varies much from day to day 
without any marked alteration in the general condition of the patient. 
In the absence of complications producing leucocytosis in pernicious 
anaemia, the leucocytes are usually diminished in number. There is a 
relative increase in the number of lymphocytes, and usually a few myelo- 
cytes may be found. 

A very rare variety of a rapidly fatal form of anaemia has been de- 
scribed in which the number of red cells is diminished without the blood 
showing the changes characteristic of pernicious anaemia. The bone 
marrow in these cases has been found to be fatty instead of hyperplastic 
as in the typical marrow of pernicious anaemia. It has been suggested 
that the bone marrow for some unknown reason had not responded to the 
call made upon it by the rapid haematolysis taking place in the disease, 
and therefore did not undergo the megaloblastic changes so character- 
istic of the bone marrow in well-marked cases of pernicious anaemia. 



LEUKAEMIA (LEUCOCYTHiEMIA). 

Leukaemia is a disease in which the characteristic changes are an alter- 
ation in the relative proportions of the different leucocytes of the blood, 
with usually an increase in their number, and the appearance of certain 
forms not seen in the circulation under normal conditions. The red cells 
are diminished in number and abnormal forms appear in the blood. 
Accompanying these alterations in the circulating blood are changes in 
the bone marrow ; less often in the spleen and in the lymph-nodes. Its 
inciting factors are still unknown. Leukaemia may be classed in three 
types, which are fairly well defined clinically and morphologically, but 
between these there exist many transitional forms, especially from the 
point of view of the morphology of the blood. These three types are the 
acute and the chronic lymphatic leukaemia and chronic myelogenous 
leukaemia ( spleno -myelogenous ) . ' 

Acute Lymphatic Leukaemia is a disease resembling clinically an acute 
infection, with a rajDidly increasing anaemia, enlargement of the lymph- 

^ Several acute cases have been reported, in which, toward the end of the disease, 
the lympliatic forms prevalent in the blood were replaced by cells containing neutro- 
phile granules, and a claim has been made for a clinical type of acute myelogenous 
leukaemia, but in view of the fact that the morphology ci the blood varies greatly a 
few days before death, and, especially as it is a matter'of experience that the lympho- 
cytes in acute lymphatic leukaemia are often very greatly diminished toward the termi- 
nation of the disease, it would seem improper to class these cases as acute myelogenous 
leukaemia. The fact that the bone marrow has not been found hyperplastic in some of 
these cases also speaks against myelogenous leukaemia. 



L 



THE BLOOD AND THE BLOOD-FOEMIXG ORGANS. 359 

nodes, and a moderate increase in the size of the spleen and liver. The 
blood changes are very characteristic. The red cells diminish rapidly 
in numbers, normoblasts are present, and the leucocytes are usually be- 
low 100, 000. The forms present are chiefly lymphocytes, either large or 
small, the large as a rule predominating. The bone marrow is altered to 
a tissue showing large numbers of lymj)hocytes, the so-called lymphoid 
hyperplasia, which often extends to the lymphoid tissue in the viscera. 

Chronic Lymphatic Leukaemia. — The blood shows a severe anaemia with 
great increase in the lymphocytes. The small forms are most abundant. 
The lymph-nodes and spleen are usually enlarged ; the bone marrow is 
in a condition of l^-mphoid hyperj^lasia, and there are Ij^mphoid infiltra- 
tions in the various organs. 

Chronic Myelogenous Leukaemia. — The blood shows a severe anaemia, 
rarelj^ of a pernicious tyi^e, with marked quantitative and qualitative 
changes in the leucocytes. The increase in number of white cells may 
be to more than one million per cubic millimetre. Myelocytes, both 
neutrophilic and eosinophilic, are quite constantly present in considerable 
numbers. They may form a large proportion of the leucocytes present. 
Mast cells are very abundant in cases of long duration. Mitoses may be 
occasionally seen in the myelocytes in rapidly advancing cases. 

The pathological forms of leucocytes in myelogenous and lymphatic 
leukaemias have little or no amoeboid motion. This explains the inter- 
esting fact that the pus from an abscess in a leukaemic subject contains 
only the polynuclear neutrophile cells found in such exudates in persons 
with a normal blood condition. In acute infections also, the number of 
myelocytes present in the circulation may be greatly reduced and the 
blood may even lose the cell forms characteristic of leukaemia, the myelo- 
cytes being replaced by the ordinary polynuclear leucocytes of normal 
type. 

The same condition may be seen in mild cases, which may under treat- 
ment reach a point in which it is difficult to make a diagnosis from the 
blood alone. 

In this connection, it must be remembered that the blood picture in 
pernicious anaemia and the leukaemias is a very variable one. As a rule, 
more than one examination is necessary for a certain diagnosis, and it 
must not be forgotten that occasionally a case, apparently of pernicious 
anaemia, may go on to a typical lymx3hatic or mj elogenous leukaemia. 

In myeloge lous leukaemia there is hyperplasia of the bone marrow, 
which usually fills the shafts of the long bones with a firm, j)ink mass 
composed largely of riyelocytes. This hyi^erplasia may involve the 
whole bone marrow of all the long bones, or it may be confined to irregu- 
lar, scattered areas, so that one should be critical in accepting reports of 
cases of leukaemia without bone-marrow changes. The other organs show 
hyperjDlasia of lymi)hoid tissue, often especially well marked in the 
gastro -intestinal tract, while scattered through the spleen are often seen 
numerous small areas containing myelocytes. 



360 THE BLOOD AND THE BLOOD-FOEMING ORGANS. 

There is some reason to think that in the spleen, for instance, some 
multiplication of the cells goes on in the so-called ^^ marrow cell or 
myeloid metastases/' In the blood, spleen, and marrow, after death, 
elongated octahedral crystals called Charcot-Leyden crystals are occa- 
sionally found. Hsemorrhages into the serous and mucous membranes 
and the retina are quite frequent, especially the latter, and fatty degen- 
eration of the viscera is a quite constant expression of the impoverished 
condition of the blood. For more detail concerning the lesions of the 
organs, see chapters on spleen, lymph -nodes, bones, etc. 



PSEUDO-LEUKEMIA. (" Hodg-kin's Disease," "Adenie.") 

Under this term it has been customary to describe a rather hetero- 
geneous group of cases characterized by progressive ansemia, by hyper- 
plasia of the lymph-nodes and nodules, with an occasional but by no 
means constant involvement of the spleen, liver, and bone marrow, and 
by new growths of lymphatic tissues in many parts of the body. While 
ansemia of moderate or severe grade is very constantly present in 
this disease, the increase of leucocytes characteristic of leukaemia is 
wanting. 

Of the exact nature of the disease (if it be a single disease) very little 
is definitely known. The enlargement of the lymjDh -nodes is in typical 
cases due to simple hyperplasia. The blood changes may present the 
type of pernicious anaemia, and in well -authenticated cases the condition 
has developed into true leukgemia. Eecent evidence favors the belief that 
some cases classed under this heading may be of an infectious character, ' 
one of the most frequently observed agents being the tubercle bacillus. 
Cases of primary sarcoma of the lymph- nodes have been described as 
cases of pseudo -leukaemia. 

The condition found at autopsy varies greatly according to the distri- 
bution and character of the new growths of lymphatic tissue. The lym- 
phatic nodules involved may be principally limited to the subcutaneous 
connective tissue (dermal type). Or the lymph-nodes of the pharynx 
and neck may be chiefly involved (tonsillar type). Or the axillary or 
inguinal or mediastinal or retroperitoneal groups may be involved. A 
somewhat charateristic condition is produced by hyperplasia, often fol- 
lowed by ulceration, of the lymph-nodules of the gastro -intestinal tract 
(intestinal type). The hyperplastic lymph-nodes may be isolated, or 
they may be joined to form large lobulated masses. The enlarged lymph- 
nodules may in the intestine project far into the lumen in spheroidal or 
polypoid form, and are sometimes dark in color as the result of the de- 
composition of haemoglobin of extravasated blood in the congested 
mucous membrane covering the nodules. Hyperplasia of the thymus has 

^ Flexner, "Multiple Lymplio- sarcomata," Johns Hopkins Hospital Reports, vol. 
iii., p. 153. 

Dietrich, Bruns' Beit. z. klin. Cliir., xvi., 1896, p. 377. 



THE BLOOD AND THE BLOOD -FORMIXa ORGANS. 361 

been described in associatiou with the lesions of the lymph-nodes. ' A 
distinct sub -variety is that which terminates in leukaemia. In general 
any of the lymph-nodes or collections of lymphoid tissue may be in- 
volved, and nearlj^ every region has been a site of origin for the new 
growths of lymi)hoid tissue, so that a great variety of combinations may 
be seen. 

The leucocytes in the blood may be slightly increased or diminished, 
and in either case the mononuclear forms are usually in excess. Myelo- 
cytes have been observed in moderate percentage, but never in such pro- 
portions as in leukaemia. "" 

ANiEMIA INFANTUM PSEUDO-LEUK-aJMICA (von Jaksch). 

This is a somewhat peculiar form of anaemia occurring in children, 
and characterized by progressive anaemia, by a considerable increase of 
leucocytes, by enlargement of the spleen and liver, and often by hyper- 
plasia of the lymph -nodes. 

By some authorities it is regarded as an early stage of leukaemia, by 
others as a form of secondary anaemia following rachitis, tuberculosis, or 
syphilis. 

The histological changes in the blood-forming organs are, so far as is 
known, very similar to, but less pronounced than, those of leukaemia. 

^ Brigidio and PiccoU, Ziegler's Beitr. z. path. Auat., Bd. xvi., p. 388. 
F. Gappert, Virch. Arcli., Bd. cxliv., 1896. Supplementlieft, p. 1. 
'■* Consult Monte and Berggriin, "Die clironisclie Anaemie d. Kindesalters," Leipsic, 
1892. 



CHAPTER II. 

THE LYMPH-NODES. 

General Characteristics of the Lymph-Nodes. 

It is well, in stud3ing the lesions of the lymph-nodes, to remember that they are 
structures so placed in the course of the lymph- vessels that the lymph, in flowing 
toward the larger central trunks, passes through them, undergoing a sort of filtration 
as it percolates through the trabeculae of the lymph sinuses. If this fact be borne in 
mind the lesions of the lymph-nodes, which are in the majority of cases secondary, are 
much more readily understood. Particles of pigment, cells from malignant tumors, 
fragments of dead or disintegrating cells either free or within phagocytes, red blood 
cells, bacteria, etc., which in any way get into the lymph-vessels, are carried along 
until a lymph -node is reached, and here they are, in part at least, deposited among the 
trabeculae of the sinuses, or are taken up by phagocytic cells, while the lymph passes on 
and out of the efferent vessels. Soluble toxic substances also are carried into the lymph 
nodes, often inciting marked and significant alterations.^ 

What is called lymphatic tissue embraces not only the so-called Ij^mph-glands and 
the less complex but still well-defined structures found in the stomach, intestines, ton- 
sils, and elsewhere, and called lymph follicles, but also the less well-defined, irregular 
masses of tissue resembling that of lymph follicles, which, as Aomold has shoAvn (Vir- 
chow's Archiv, Bd. Ixxx., p. 315; Bd. Ixxxii., p. 394; Bd. Ixxxiii., p. 289; Bd. Ixxxvii., 
p. 114), is widely disseminated in variable amounts in different parts of the body; in 
the lungs, beneath the pleura, in the interlobular septa, and elsewhere ; in the liver, 
kidneys, etc. Although the exact nature of these more diffuse masses of lymphatic 
tissue is too little understood, as indeed is that of the lymph follicles and glands them- 
selves, there is reason to believe that they are analogous structures and prone to be 
affected by similar deleterious agencies. It seems better, in view of the fact that the 
so-called lymph-glands are not glands at all, in the ordinary sense of the word, to call 
them lymph-nodes, and the smaller masses of lymphatic tissue scattered through various 
parts of the body lymph-nodules instead of "lymph follicles." 



ATROPHY. 

Atrophy is a very regular occurrence in old age. In this condition 
the nodes are small, hard, and, unless pigmented, light in color. Micro- 
scopical examination shows a marked diminution in the number of par- 
enchyma cells, while the reticulum and the capsule and trabeculae may be 
thickened. There may be an accumulation of fat around the node in 
senile atrophy. 

It should be remembered, in this connection, that the lymph-nodes, 
as well as the lymphatic tissue in general, in children are more volumi- 
nous than in adults. 

^ For a studv of bacteria in normal lymph-nodes see Kdlble, Mlinch. med. Wochen- 
schr., 1899, p. 622. 



THE LYMPH-NODES. 



363 



DEGENERATION. 

Amyloid Degeneration of the blood-vessels and reticulum of the lymph 
nodes occurs under the conditions which favor this change in general. 
It may occur in connection with amyloid degeneration of other parts of 
the body, or by itself. It may occur in nodes otherwise normal, or in 
those which are the seat of other lesions — thus in simple chronic or tuber- 
culous inflammation. It is frequently found in the mesenteric lymph- 
nodes, in connection with waxy degeneration of the intestinal mucous 
membrane. 

Hyalin Degeneration of the external layers of the smaller arteries and 
the capillaries and reticulum of the lymph-nodes occurs occasionally in 
old age or in connection with wasting diseases. 

PIGMENTATION. 

The pigment which is very frequently found in lymph-nodes may be 
derived from the hgemogiobin of the blood, either in the nodes themselves 
or in remote parts, or it may be formed of various materials introduced 




Fig. 193.— Pigmentation of Bronchial Lymph-Node. 

The pigment is largely in the lymph sinuses and enclosed in cells. A, Capsule of node ; B, lymph follicle 
— nodule; C, perifollicular lymph sinuses. 



into the body from without, such as the pigments used in tattooing, re- 
spired dust particles of various kinds — coal, stone, iron, etc. (Fig. 192). 
The pigment particles, which usually first lodge in the lymph sinuses, 
may collect here in large quantities, either in the reticulum or the cells 
lying in its meshes ; they may penetrate the follicles and cords and find 
permanent lodgment there. They usually induce a greater or less degree 
of chronic inflammation, so that in extreme cases, such as are frequently 
seen in the bronchial lymph-nodes, nothing is finally left of the node but 



364 



THE LYMPH -NODES. 



a more or less deeply pigmented mass of dense connective tissue. The 
function of the node may be, of course, in this way partially or entirely 
destroyed. The pigment in these cases appears to reach the node, in 
part by being carried along free in the lymph current, in part through 
transportation by leucocytes in which the i3articles have become enclosed. 
Pigmentation of the nodes is most marked in those about the root of the 
lungs, which are frequently of a mottled gray or a black color, but it 
may occur in the mesenteric and other nodes. Under similar conditions 
the diffuse lymphatic structure in the lungs and liver may be pigmented. 

INFLAMMATION. 

Acute Inflammation of the lymph- nodes is commonly due to the pres- 
ence of pathogenic micro-organisms or of toxic substances, usually bac- 
terial in origin, which may be formed in the node or brought to it in the 




Fig. 193.— Acute Hyperplastic Inflammation of Lymph-Node in Typhoid Fever. 

Showing a portion of one of ttie mesenteric nodes. A, Capsule ; B, perifollicular space or lymph sinus, 
containing in its meshes many large cells ; C, portion of one of the follicles, with large and small cells in 
the meshes of its reticulum. 



lymph current from the tributary region of the body. Under these con- 
ditions the nodes are usually swollen, reddened, and softer than normal, 
and are often the seat of small hsemorrhages. One or all of the nodes of 
a cluster may be affected. 

Two forms of the acute inflammatory process may conveniently be 
recognized, an hyperplastic and an exudative. 

In the HYPERPLASTIC form a microscopical examination shows the 
lesion to be largely due, in addition to the hypergemia and haemorrhage, 
to a proliferation of the cells of the node ; the spheroidal mononuclear 



:>f¥ 



"it 



THE LYMPH-NODES. 365 

cells of the nodules (^'follicles '') and cords, and especially the endothelial 
cells of the lymj)h spaces (Fig. 193), which may increase in number and 
exfoliate to such an extent as to fill and largely distend the lymj)h 
sinuses. These endothelial cells often contain red blood cells, leucocytes, 
and fragments of other cells (Fig. 194). In typhoid fever, as well as in 
many other infectious diseases, necrosis of the hyperplastic tissue is com- 
mon (see p. 206). 

After simple hyi)erx)lasia of the lymph-nodes, resolution readily oc- 
curs. But if necrosis have taken place, such areas may be replaced by 
fibrous tissue. 

This form of lesion of the lymph-nodes is common. It may occur in 
the cervical nodes with many forms of angina ; in the inguinal nodes in 
connection with acute infec- 
tious processes in the external * ^^^ .-^- 
genital organs ; in the axilla < '-^ i ^.'^v^^^^w 
with infectious processes in the 
hand, arm, or breast; in the 

mesenteric nodes with infection ^ ,^ 

or intoxication of intestinal or ^W-^. 

other origin. Similar lesions - ^ m-, 2: (ik'\'« 

occur in the solitary lymph • ''/' 

nodules and Peyer's patches of 
the intestine (Fig. 195). ' . ** 

In EXUDATIVE or SUimura- ^^^- 194.— endothelial cells IX Hyperplasia of 
. . „ -. • ,1 , • n THE Lymph-Nodes. 

Uve lorms oi intiammation ol 

■ T T ^ T . T Ti- The exfoliated cells contain red blood cells, fat droplets, 

the lymph-nodes, m addition and masses of wood pigment. 

to the simple hyperplastic 

changes just described, there are emigration and collection of leucocj^tes, 
with the formation of more or less fibrin in the lymph sinuses as well 
as in the interstices of the nodules. The capsule of the nodes may be 
infiltrated with exudate. With these changes there may be necrosis and 
softening of the tissue of the nodes and the development of abscesses. 
Small abscesses may coalesce, and thus a considerable part of the node 
is converted into a suppurating necrotic mass — hubo. Such a bubo may 
open externally or into the surrounding tissue and heal by granulation 
tissue and cicatricial tissue ; its contents may be absorbed or become 
dry and dense and calcified, and surrounded by fibrous tissue. Suppu- 
rative inflammation of the lymph- nodes often occurs in connection with 
supj)urative processes elsewhere, in pyaemia, venereal infection, etc. 

The lymph-nodes of children are, as a rule, more readily involved in 
infectious processes of other parts than are those of adults. 

Chronic Inflammation. — This is characterized by the increase of the 
connective-tissue elements of the node, with a gradual and commensurate 
disapx)earance of the lymphoid cells. The reticulum of the follicles and 
sinuses becomes thickened and fibrous, and in the trabeculse and capsule 
new connective tissue is formed, until, in advanced cases, the entire node 
may be more or less extensively converted into a mass of fibrous tissue. 



366 THE LYMPH- NODES. 

This condition is very frequently seen in the lower tracheal and in the 
bronchial nodes, apparently as a result of the lodgment in them of re- 
spired pigment particles ; but it may occur in any nodes, either as a result 
of repeated moderate degrees of inflammation or from causes which we 
do not know. In some cases the nodes are greatly enlarged and the 
new tissue contains many large cells, while in other cases the connective 
tissue is dense and contains but few cells (Fig. 196).' 

Tuberculous Inflammation may be local, confined to the nodes, or it 
may occur in connection with general acute miliary tuberculosis, or with 

- ,/ ^» ^r^ .-; .>-4.^ J 









Fig. 195.— Hyperplasia of Peyer's Patch in Typhoid Fever. 
Showing new-formed endothelial cells in the meshes of the reticular tissue between the blood-vessels. 

tuberculous inflammation of single organs. It may occur in single nodes, 
or in several nodes of the same group, or in groups situated in different 
parts of the body. In its simple and acute form there may be no evi- 
dent change to the naked eye in the appearance of the nodes, or they may 
be besprinkled with small, grayish-white, translucent spots. Under these 
conditions the nodes may be reddened and soft, or swollen and denser 
than normal. In more advanced forms of the lesion the tubercles coalesce 
and undergo a greater or less degree of cheesy degeneration. Under 
these conditions the cheesy areas are evident to the naked eye as more or 
less shari3ly circumscribed, opaque, whitish or yellowish areas, frequently 
surrounded by an irregular, more translucent, grayish zone of tubercle 
tissue which merges insensibly into the adjacent tissue. The entire node 
may become involved, and more or less completely converted into a 
cheesy mass, in the periphery of which a zone of tubercle tissue may or 
may not be evident. 

Microscopically the small nodules or miliary tubercles are seen to 
consist of more or less circumscribed collections of small spheroidal, or 
more frequently larger polyhedral cells, with or without well-defined 
giant cells. They usually commence to form in the follicles and lymph 
cords of the nodes, and from these may spread and involve the entire 
surrounding tissue. The cheesy degeneration, which here as elsewhere is 
apt first to involve the central portions of the tubercles, presents the 

' Consult Eibbert, "Ueber Regeneration und Entziindung der Lymplidriisen, " Zieg- 
ler's Beitrage zur path. Anat., Bd. vi., p. 187, 1889. 



THE LYMPH-NODES. 



367 



usual appearances. Tubercle bacilli may be found in the edges of the 
cheesy areas or in the tubercle tissue about them. 

Simple inflammatory changes regularly occur in the periphery of the 
tubercles. There is an increase of cells in the lymi)h sinuses and follicles, 
and a more or less marked swelling, and apparently a proliferation of the 
cells of the reticular tissue of the node. In cases in which the process is 
chronic there is often marked increase of the connective tissue of the 
nodes, the reticular tissue becomes dense and fibrous, and the trabeculse 
and capsule are thickened. The tubercles themselves, instead of under- 
going cheesy degeneration, may become fibrous or be converted into a 
hyalin material. 

The cheesy material may dry and shrink, and become enclosed by a 
capsule of dense connective tissue and become calcified ; or it may soften, 
and thus cavities be formed in the nodes, filled with grumous material ; 
or inflammatory changes may be induced in the vicinity of the nodes, 
leading to abscesses. On the other hand, hyperplastic inflammation in 




Fig. 196.— Chronic Inflammation of Bronchial Lymph-Node. 

Sbowing obliteration of the lymph sinuses and atrophy of the lymph-nodules hy the new-formed connective 

tissue. 



the i^erix^hery of the affected nodes may result in their becoming bound 
together into a dense nodular mass. 

Scrofula. — Tuberculous inflammation of the lymph-nodes, especially 
in those of the cervical,' bronchial (Plates iii. and xi. ), and mesenteric 
groups, often occurs in children, particularly in those who are ill -nour- 
ished. I^orthrup and Bovaird found in an analysis of 200 cases of tu- 
berculosis in children that the lungs and bronchial lymph -nodes were 

^ For bibliography of cervical tuberculous lymph-nodes see J)owd, Annals of Sur- 
gery, May, 1899. 



368 THE LYMPH- NODES. 

involved in 148. ' Such persons, in addition to the lesion of the lymph- 
nodes, are very liable to suffer from chronic tuberculous and other in- 
flammations of the mucous membranes, skin, periosteum, joints, and the 
subcutaneous and other connective tissues. This general condition is 
known as scrofula, and the lesion of the nodes is sometimes called scrofu- 
lous infla mmation. 

While in many cases the portal of entry of the tubercle bacilli is not 
evident, and the lesions often present the appearance of hyperplasia of 
the lymphoid tissue with cheesy degeneration and the formation of more 
or less dense fibrous tissue rather than the typical characters of tubercu- 
lous tissue, nevertheless, miliary and other forms of tuberculous inflam- 
mation are often present in so-called scrofula, and tubercle bacilli, while 
sometimes absent, are often present and virulent.'"^ 

The necrotic portions of such cheesy lymph-nodes in scrofula may 
soften and break down, and by the establishment of purulent and necrotic 
inflammation about them abscesses may form which may open externally. 
These abscesses may heal ; but usually the healing is difficult and slow, 
and long-continued suppurations, frequently with the development of 
fistul?e, are very common. Instead of softening, the cheesy material in 
the nodes may become dry and hard and undergo calcification. 

Generalized Tuberculous Lymphadenitis. — Several cases have 
been recorded of extensive tuberculous hyperplasia of the lymph-nodes 
in various parts of the body, the lesion resembling in its gross characters 
that of pseudo-leuksemia. AYhile in some of these cases the morphology 
of the lesions is characteristic of tuberculosis, in others the new tissue is 
diffuse and consists largely of new-formed sraall spheroidal and poly- 
hedral cells with large multinuclear cells and of fibrous tissue. The new- 
formed cells may undergo necrosis. Thus the tuberculous nature of the 
lesion is not always plain even on microscopic examination. Animal 
inoculations are often necessary for the establishment of the nature of 
such cases." 

Syphilitic Inflammation. — The lesions of the lymph-nodes which occur 
in connection with syphilis vary greatly, depending upon the stage of the 
disease. In the primary stage the nodes in the region of the seat of in- 
fection are apt to present the lesions of an ordinary acute inflammation, 
frequently with suppuration. 

In the secondary stage of the disease the nodes of other regions, neck, 
elbow, axilla, etc., are often sw^ollen and hard. On microscopic exam- 
ination there may be an increase of connective tissue in the capsule and 
trabeculae, but the chief change is in the accumulation in the follicles and 
lymph sinuses of larger and smaller spheroidal and polyhedral cells. 

^ For a consideration of tlie significance of tuberculous bronchial lymph-nodes in 
children, consult Northrup, New York Medical Journal, February 21, 1891 ; also 
Bovaird, ibid., July 1, 1899. See further, reference to Marfan, p. 443. 

'^ For a full bibliography of scrofula see Cornet, in Kothnagel's " Specielle Pathologic 
u. Therapie," Bd. xiv., Th. iv. For a study of variations in virulence in tubercle ba- 
cilli in scrofulous and other tuberculous lesions see Lartigau, Jour. Exp. Med., vol. vi. 

^ For a study of this form of tuberculosis, consult Crowder, New York Medical 
Journal, September 15th and 22d, 1900, bibl. 



THE LYMPH-XODES. 369 

The reticular tissue may be thickeued aud the walls of the blood-vessels 
infiltrated with cells. lu this condition the nodes may remain for a long 
time, not tending to form abscess; or they may undergo resolution 
through degeneration and absorption of the cells. 

In the tertiary stage of the disease the nodes may be the seat of chronic 
inflammation characterized by the formation of gummata. Under these 
conditions they may form large, firm nodular masses from the gro^^ng 
together bj^ new connective tissue of several altered nodes. The gross and 
microscopical characters of gummata of the Ij^mph-nodes are, in the main, 
similar to those in other iDarts of the body. 

HYPERPLASIA OF THE LYMPH-NODES. (Lymphoma.) 

In addition to the considerable enlargements of the lymi3h- nodes in in- 
flammation which have been described above, they become enlarged under 
a variety of conditions which we do not understand. This lack of knowl- 
edge of the etiology, together with our ignorance of certain functions of 
the lymph-nodes, and the morphological similarity, or even identity, 
which these enlarged nodes present under various conditions, render it 
very difficult to decide upon the exact nature of the change, and in many 
cases to distinguish one form of enlargement from another. 

In the first place, there is a class of cases in which, sojnetimes slowly, 
sometimes with great rapiditj', the lymph -nodes of certain regions, espe- 
cially the abdominal, axillary, cervical, and inguinal, enlarge, not in- 
frecxuentlj" to an enormous extent. They may be either hard or soft, even 
almost fluctuating ; the individual nodes may be distinct or merged into 
one another. Sometimes the nodes in nearly all jDarts of the body are 
affected. Microscopic examination shows, in the soft varieties, a large in- 
crease of small spheroidal and polyhedral cells and a growth of the retic- 
ular tissue. It is a new formation of lymphatic tissue, but the normal 
relations of follicles, cords, and lymjDh sinuses are not preserved. In the 
harder varieties there is a thickening of the reticular tissue in addition to 
an increase of cells. In rare cases portions of the nodes become necrotic. 
Sometimes larger and smaller haemorrhages occur in the nodes, especially 
in the softer forms. In addition to these changes in the lym^Dh-nodes 
there is, in a considerable j)rox)ortion of cases, a new formation of lymph- 
atic tissue in greater or less quantity in other parts of the body, in the 
spleen, in the gastro -intestinal canal, in the marrow of bones, in the liver, 
kidneys, etc. , and the number of lymphocytes in the blood and in other 
parts of the body is increased. This general condition is known as 
Jeul-cemia and has been considered above, under diseases of the blood and 
blood-forming organs. The enlarged lymj)h-nodes in this disease may 
be called, for convenience, leiikcemic ly^nphomata. 

In the second i^lace, there is a form of disease resembling leukaemia 

in many respects, particularly in the lesion of the lymj)h-nodes, usually 

with a less prominent involvement of the spleen and other lymphatic 

structui^es, and, which is more striking, no increase in the number of 

24 



370 THE LYMPH-NODES. 

leucocytes in the blood. This is called Hodgkin^s disease, or pseudo-Jeu- 
kcemia, aud the enlarged lymph-nodes may in this case be called jyseudo- 
leukcemic lymphomata. The lesions of the lymph -nodes are apparently 
similar in both diseases, but it is convenient to assign different names to 
them because they seem to arise under different conditions and to be 
associated with a constant difference in the character of the blood. 
There is some reason for the conjecture that Hodgkin's disease may be 
infectious in its nature. Whether the pyogenic cocci and the xDueumo- 
coccus which have been found in the lesions are the excitants or not is 
not yet certain. 

Le Count has recently described a benign tumor — lymphoma — in the 
groin having the structure of a lymph-node.' A form of generalized 
tuberculous lymiihadenitis which may be mistaken for Hodgkin's dis- 
ease is described above. 

TUMORS. 

Sarcoma occurs in the lymph-nodes as a primary and secondary tumor, 
and may be of various forms: spindle- celled, large and small round- 
celled, and angio- sarcoma. It is not easy in many cases to distinguish 
morphologically between the small round- celled sarcomata and the above- 
described lymi)homata, but in general the leuksemic and pseudo-leukgemic 
lymphomata remain circumscribed, while the sarcomata tend to break 
through the node capsule and invade the surrounding tissues. Fibroma, 
myxoma, and chondroma occur in the lymph nodes, but are rare. Endothe- 
liomata are described, but are not common. Secondary carcinomata are 
of frequent occurrence, the form of the cells and the nature of their 
growth depending upon the seat and character of the primary tumors. 

PARASITES. 

Aside from the various forms of bacteria which are not infrequently 
found in the lymph-nodes in infectious diseases, among the animal para- 
sites filaria, trichina, and pentastomum have been described. 

^ Jour. Exp. Med., vol. iv., p. 559, bibliography of lymphoma. 



CHAPTER III. 

THE SPLEEN AND THYMUS. 

The Spleen. 

General Characteristics of the Spleen. 

In studying the lesions of the spleen it is important to bear in mind the peculiar 
relations in which this organ stands to the blood-vessels and to the circulation. After 
passing through the various branches of the splenic artery and the limited systems of 
capillaries which are associated with it, the blood is not received at once into venous 
trunks, as in other parts of the body, but is poured directly into the pulp tissue. In 
this it circulates, under conditions which render it liable to stagnation and undue accu- 
mulation, before it is taken again into well-defined vessels through the open walls of 
the cavernous veins. Moreover, these conditions, naturally unfavorable to undisturbed 
and vigorous circulation, are reinforced by the association of the splenic with the slug- 
gish and often interrupted portal circulation. Bearing these considerations in mind, it 
is in a measure plain why, as is in fact the case, the spleen should be more liable to 
alterations in size than any other organ in the body, and why, serving as it does as a 
sort of blood filter, it should be especially susceptible to the influence of deleterious 
materials of various kinds which in one way or another gain access to the blood. The 
relationship between the lymph-vessels and the spleen is also intimate. 

Malformations and Displacements. 

The spleen may be absent in acephalous monsters, and with defective development 
of other abdominal viscera. Absence of the spleen in otherwise normally developed 
individuals has been recorded. There may in this condition be a compensatory hyper- 
plasia of the Ij^mphatic tissues of the body.^ Small accessory spleens, from the size of 
a hazelnut to that of a walnut, are not infrequent. They usually lie close to the spleen, 
but may be at a considerable distance from it ; thus they have been found embedded in 
the head of the pancreas. Two spleens of about equal size have been observed. The 
form of the spleen is subject to considerable variation. It may be made up of several dis- 
tinct lobes. It may be displaced congenitally or as the result of disease. It may be on 
the right side in transposition of the viscera. As the result of congenital defects in the 
diaphragm the spleen may be found in the thorax ; or in deficient closure of the abdomi- 
nal wall it may, together with other abdominal viscera, be found ovitside of the body. 

The spleen may be pressed downward by any increase in the contents of the thorax. 
It may be bound by adhesions to the concave surface of the diaphragm, so that its long 
axis is nearly horizontal instead of vertical. It may be displaced by changes in the 
contents of the abdominal cavity. If the organ be increased in size it frequently be- 
comes tilted, so that its lower border reaches the right iliac region. If the ligaments be 
too long congenitally, or if they are lengthened by traction, and if the organ is at the 
same time increased in weight, it ma}^ become very movable. It may sink downward, 
with its hilus turned upward ; or it may be rotated on its axis, and, owing to torsion of 
the vessels thus produced, the organ may atrophy ; or the pressure of the ligaments 
and vessels across the duodenum may cause occlusion of the gut. 

1 See Hodenpyl, Med. Record, November 12th, 1898, bibl. 



372 THE SPLEEN AND THYMUS. 



WOUNDS, RUPTURE, AND H-ffiMORRHAGE. 

Wounds of the spleen are usually accompanied by extensive hsemor- 
rhage and are commonly fatal. Death usually occurs as the result of 
this haemorrhage, but it may be due to secondary inflammatory changes. 
Healing and recovery may, however, occur. 

Rupture of the spleen may be traumatic or spontaneous. In the 
former case it may be due to direct violence in the region of the organ 
or to injury to the thorax, falls, etc. In certain diseased conditions the 
spleen is more liable to ruiDture than when it is normal. The rupture 
usually involves not only the capsule, but a more or less considerable 
portion of the parenchyma, and of course leads to haemorrhage. Spon- 
taneous ruj)ture is rare, but may occur in excessive enlargement of the 
organ, as in tyj)hoid fever, malaria, etc. — see below — or as the result of 
abscess. 

Hgemorrhage. — Aside from the extensive haemorrhages from injury and 
rupture, the spleen may be the seat of small circumscribed haemorrhages 
in various infectious diseases, although, owing to the peculiar distribu- 
tion of the blood, it is often very difficult to distinguish between a mod- 
erate interstitial haemorrhage and hyperaemia. Sacculated aneurism of 
the splenic artery has been reported. 



ATROPHY. 

Atrophy of the spleen may occur in old age; as a. result of prolonged 
cachexiae, and in connection with profound and persistent anaemia ; or, 
more rarely, from unknown causes. The capsule may be wrinkled and 
thickened, the color pale, the trabeculae i^rominent, the consistence in- 
creased. The change is largely in the pulp, whose parenchyma cells 
are decreased in number. 

DEGENERATION. 

Amyloid Degeneration. — This may affect the glomeruli or the pulp 
tissue, or both together. When confined to the glomeruli the spleen may 
or may not be enlarged, and the cut surface is more or less abundantly 
sprinkled with round or elongated, translucent bodies resembling consid- 
erably in general appearance the grains of boiled sago. These are the 
waxy glomeruli. Such a spleen is often called ^^sago spleen ^' (Fig. 197). 
Microscopical examination shows that the degeneration is confined to the 
walls of the arteries, capillaries, and reticulum of the glomeruli, with 
atrophy and often finally total disappearance of the lymphoid cells. 

In other cases, either with or without involvement of the glomeruli, 
there is waxy degeneration of the blood-vessels and reticulum of the 
pulp, which may occur in patches or be general and more or less ex- 
cessive. If the alteration is general and considerable the spleen is en- 
larged, its edges are rounded, its consistence is increased. On section it 



THE SPLEEX AXD THYMUS. 373 

appears translucent, and the distribution of the degenerated areas may be 
readily seen by holding a thin slice up to the light. The spleen may be 
alone affected, or there may be similar degenerations in other organs. 

PIGMENTATION. 

This may occur as the result of the decomposition of haemoglobin in 
the organ or elsewhere, under a great variety of conditions : thus after 
hcTinorrhagic infarctions, small multiple haemorrhages, acute hyiDcrplastic 
splenitis, and in hsemachromatosis, etc. Or the pigment may be anthra- 
cotic and be brought to the organs from the lungs or bronchial nodes ; 



Fig. 197.— Amyloid Degeneration of the Glomeruli of the Spleen— "Sago Spleen." 

bile pigment may also be deposited in the spleen in jaundice. The pig- 
ment may lie in the walls of the smaller arteries, in the cells and reticu- 
lum of the pulp, or free in the latter tissue, or in the follicles. It is 
usually quite unevenly distributed. The pigment may be red, brown, 
or black. According to Weigert anthracotic pigment may be sometimes 
seen with the naked eye in the periphery of the glomeruli as dark 
crescents. 

DISTURBANCES OF THE CIRCULATION. 

Anaemia. — This may be associated with general ansemia, but it is not 
alwaj'S present in this condition. Allien marked and unassociated with 
other lesions the spleen is apt to be diminished in size, the capsule more 
or less wrinkled, the cut surface dry and lighter in color than normal, 
the trabeculee unduly j)rominent. 

In this, as in other alterations simply of the blood content of the 
spleen, neither the gross nor microscopical appearances are constant, be- 



374 



THE splee:n^ and thymus. 



cause of the redistribution of blood which is apt to occur in the viscera 
after death. 

Hyperaemia. — Passive hyperemia may occur in obstruction to the 
portal circulation, most frecxuently in cirrhosis of the liver, but also 
with certain valvular lesions of the heart, emphysema, etc. The spleen 
is enlarged, but usually only to a moderate degree. The capsule is apt 
to be tense, and on section the pulp is dark-red and may be soft or firm. 
The cavernous veins are dilated (Fig. 198). Usually, when the lesion 
has existed for some time, there is a thickening of the trabecules and 
reticular framework of the spleen, so that these are prominent on section. 




Fig. 198.— Hyperemia— Coxgestion—of the Spleex. 



b, Dilated cavernous veins ; c, trabecula of pulp tissue compressed between dilated cavernous veins ; d, 

glomerulus. 

In other words, there is a chronic interstitial splenitis following the 
chronic congestion. 

Active Hypee.emia of the spleen, which in most cases is scarcely 
to be differentiated from some forms of acute inflammation, and probably 
in many cases is associated with it, very frequently occurs in a great 
variety of acute and infectious diseases, such as tj'phoid fever, pneu- 
monia, diphtheria, pyaemia, the exanthemata, etc. The spleen is en- 
larged, the cax)sule tense ; on section the pulp is soft, dark -red in color, 
often swelling out from the cut surface and concealing the glomeruli and 
trabeculee. Under these conditions the cavernous veins are distended 
with blood and the interstices of the pulp infiltrated with a variable, 
sometimes large quantitj^ of red and white blood cells. Or, in addition 
to this, there may be hyperplasia (see below). 

Embolism and Infarction of the Spleen. — Embolic infarctions of the spleen 
are of frequent occurrence. They may be single or multiple, small or 
very large, sometimes occupying half of the organ. They are in general 
approximately wedge-shaped, corresponding to the area of tissue sup- 



THE SPLEEN AND THYMUS. 375 

plied by the occluded artery (Fig. 14, j). 76). They may be hgemor- 
rhagic, l. e. , red, or they may be white. Infarctions, originally red, may 
become white after a time from changes in the blood i^igment. They may 
usually be seen as dark-red, reddish-white, or w^hite, hard, sometimes 
slightly x)r ejecting areas on the surface of the organ. ^N^ot infrequently 
the centre of the infarction is light in color, while the peripheral zone is 
dark -red. A layer of fresh fibrin is sometimes seen over the surface of 
the infarction. The general as well as the microscopical appearances 
which they present depend largely upon the age of the infarctions. In 
the earlier stages the hsemorrhagic infarctions present little more under 
the microscope than a compact mass of red blood cells, among which 
may be seen the conix)ressed parenchyma. The white infarction may 
show at first an outline of the splenic structure, but the entire tissue is 
in a condition of coagulation necrosis. The tissue may disintegrate and 
soften, and be more or less comx^letely absorbed, with or without fatty 
degeneration. A zone of inflammatory tissue may appear around the 
infarction and upon the capsule, and this tissue, becoming denser, as- 
sumes the characters of a cicatrix and contracts ai'ound the unabsorbed 
remnant of the infarction, so that finally nothing may be left but a dense 
mass of fibrous tissue, which frequently draws in the surface, causing 
more or less distortion of the organ. This cicatrix may be pigmented or 
white. 

If the embolus be infective, in addition to its mechanical effects there 
may be sui)puration, gangrene, and the formation of abscess. There 
may be perforation of the capsule and fatal peritonitis. Infarctions of 
the spleen may follow thrombosis of the splenic vein. 

Thrombosis of the splenic vein is rare as a primary lesion, but it 
may be of secondary occurrence in connection with portal or mesenteric 
thrombosis, with other lesions of the spleen, or with acute inflammation 
of the iDancreas. Thrombosis of the splenic vein has been reported fol- 
lowing typhoid fever. 

INFLAMMATION. 

Inflammatory Hyperplasia" (Acute Hyperplastic Splenitis, Acute Splenic 
Tumor). — The conditions under which hyperplasia and acute inflamma- 
tion of the spleen occur have already been mentioned under active 
hypersemia, with which it is usually associated. It is a frequent though 
not a constant accompaniment of the acute infectious diseases. The 
spleen is enlarged, sometimes to two or three times its normal size. On 
section the pulp is soft, often almost diffluent, and projects upon the cut 
surface. The color is sometimes dark-red, sometimes grayish-red, or 
mottled red and gray. The trabecul?e and glomeruli are usually concealed 
by the swollen and softened pulp, but the glomeruli are sometimes 
unusually prominent. 

Microscopical examination shows the marked increase in size to be 
due in part to the hyperfemia ; in part to a swelling and increase in the 
number of cells, sometimes of the pulp, sometimes of the glomeruli, or 



376 THE SPLEEN AND THYMUS. 

of both. There are multinuclear cells ; cells resembling the ovoidal aud 
polyhedral cells of the pulp, but larger and with evident division of the 
nuclei. Cells resembling leucocytes niay be present in large numbers, 
and larger and smaller cells in a condition of fatty degeneration, or con- 
taining pigment, are often seen. The elongated cells lining the cavernous 
veins may be swollen or increased in number. Not infrequently the larger 
and smaller cells contain red blood cells or their fragments. In some 
cases, particularly in scarlatina, hyperplasia of the glomeruli is a prom- 
inent feature : in other cases, particularly in typhus and recurrent fevers, 
the cells of the glomeruli undergo marked degenerative changes, so that 
they may form small softened areas looking like little abscesses. Focal 
necroses and areas of small-celled accumulation or cell i)roliferation are 
common in typhoid fever and other infectious diseases (see page 178). 
As the primary disease runs its course the swelling of the spleen sub- 
sides, the capsule appears wrinkled, the color becomes lighter, and 
sometimes the organ remains for a long time, or permanently, small and 
soft. 

The lesions of the spleen are in mauy cases due to the presence of 
micro-organisms which are usually present in the spleen in septicaemia, 
or they may be due to soluble toxic substances in the blood. ' 

Suppurative Splenitis {Splenic Abscess) . — Small abscesses may be found 
in the spleen as the result of minute infectious emboli, and these may 
coalesce to form larger abscesses. Sometimes the entire parenchyma is 
converted into a soft, necrotic, purulent mass surrounded by the capsule. 
It is rare for simi)le infarctions to result in abscess. Abscess of the 
spleen may occur from the propagation of a suppurative inflammation to 
the organ from adjacent parts ; from perinephritic abscesses, ulcer and 
carcinoma of the stomach, etc. They may open into the peritoneal cav- 
ity, inducing fatal peritonitis, or, owing to an adhesive inflammation, 
the Oldening may occur into the post -peritoneal tissue, into the pleural 
cavity, lung, stomach, intestines, or it may open on the surface. On the 
other hand, the contents of the abscess may dry, shrink, and become 
encapsulated and calcified. Abscesses may occur in ulceratiA^e endocar- 
ditis, X3y{]emia, typhoid fever, and more rarely in intermittent fever, and 
under a variety of other conditions. 

Chronic Indurative Splenitis (Chro7iic Splenic Tumor). — There may be, 
as we have already seen, a new formation of connective tissue in the 
spleen as a result of chronic congestion or infarctions, or about abscesses. 
But there is a more diffuse formation of connective tissue, usually in the 
nature of an hyperplasia, which occurs under a variety of conditions, 
and is now marked and extensive, and again comparatively ill-defined. 
It is always associated with more or less extensive changes in the paren- 
chyma. In its most marked form it is found in chronic malarial poison- 
ing, and under these conditions it may be found not only in persons who 
have suffered from repeated attacks of intermittent fever, but also in 

' For a study of the role of the spleen in infections see Courmont and Buffau, 
Arch, de Med. Exp., t. x., p. 431, 1898, bibl. 



THE SPLEEJs^ AND THYMUS. 



377 




those who have not thus suffered but have resided in malarial regions. 
The enlarged spleen is often called '^ague cake." Similar conditions, 
though usually less marked, may occur in congenital and acquired syphi- 
lis, from jjrolonged typhoid fever, and as a result of acute hyperiDlastic 
splenitis from various causes, and also inleuksemia and pseudo-leuksemia. 

The gross appearance of the spleen in chronic indurative splenitis 
varies greatly, both in the size of the organ and in the appearance of the 
section. The spleen may be enormously enlarged or it may be of about 
normal size. It is usually, however, enlarged. The cai)sule is commonly 
more or less thickened, frequently unevenly so. The consistence is 
as a rule considerably increased, but this is not always the case. The 
color and appearance of the cut surface present much variation. It may 
be nearly normal or it may be grayish, or 
dark brown, or nearly black. The color 
may be uniform or the surface may be 
mottled. The glomeruli may be scarcely 
visible or very prominent ; the trabecuhe 
are in some cases nearly concealed by the 
pulp ; in others they are large, prominent, 
and abundant, so that the surface is crossed 
in all directions by an interlacing network 
of broader and narrower irregular bands, 
between which the red or brown or black- 
ish pulp lies. 

^ot less varied are the microscopical 
appearances of the spleen under these con- 
ditions. In one class of cases there is 
more or less uniform hyperplasia of both pulp and interstitial tissue. 
The parenchyma cells are increased in size and number ; there may be 
swelling and proliferation of the lining cells of the cavernous veins (see 
Fig. 199). The reticulum of the pulp, as well as that of the glomeruli, 
and also the trabeculae, are thickened. In another class of cases the 
thickening of the reticular and trabecular tissue, either uniformly or in 
patches, is the prominent feature (Fig. 200), while the changes in the 
pulp are rather secondary and atrophic. In both forms irregular pig- 
mentation is frequent, the pigment particles being deposited either in the 
cells of the pulj) or glomeruli, or in the new-formed interstitial tissue (Fig. 
201). Finally, there are all intermediate forms of induration between 
those described, and the changes are by no means uniform in the same 
organ. When these spleens are large they are liable to displacement. 

Syphilitic Splenitis. — This lesion may present itself as an indurative 
process due to the formation of new connective tissue, and present no dis- 
tinct morphological characteristics. In rare cases, however, gummata 
may be present in connection with the new fibrous tissue ; then the nature 
of the lesion is evident. 

Tuberculous Splenitis. — This lesion is usually secondary to tuberculous 
inflammation in some other part of the body, or is the result of the gen- 



FlG. 199. 



Chroxic Indurative Splen- 
itis. 



Showing swelling and proliferation of the 
lining cells of the cavernous veins. 



378 



THE SPLEEN AND THYMUS. 



eral infection in acute general miliary tuberculosis. The tubercles may 
be very numerous and still invisible to the naked eye, or they may be 
just visible, or as large as a pin's head, and very thickly strewn through 




Fig. 200.— Chronic Interstitial Splenitis. 

a. Thickened capsule ; b, thickened trabecule ; c, dilated cavernous veins ; d, dense pulp tissue with 

obliterated cavernous veins. 



the organ or sparsely scattered. In other cases the tubercles are larger, 
sometimes as large as a pea, and they are then usually not numerous. 
Microscopically they present the usual variety of structure, sometimes 
as simple tubercle granula, sometimes as conglomerate tubercles ; they 
may consist simply of a collection of small spheroidal cells, or there may 
be larger polyhedral cells and giant cells with a well-defined reticulum. 

Cheesy degeneration occurs under the usual 
conditions. Tubercle bacilli are usually pres- 
ent, particularly in the more acute forms, 
sometimes in small, sometimes in enormous 
numbers. They seem to be especially abun- 
dant in acute general miliary tuberculosis of 
children. These tubercles may be formed in 
the glomeruli, in the walls of the smaller 
arteries, in the pulp tissue, and in the trabec- 
ulce and capsule. Owing to the peculiar 
character of the spleen tissue the earlier 
stages are not readily recognized, since simple 
collections of small spheroidal cells are not 
distinctly outlined against the normal tissue. 
There is frequently a moderate swelling of the spleen, owing to hyper- 
8emia and hyperplasia of the parenchyma. 

Perisplenitis. — Acute Inflammation of the capsule of the spleen 
may occur as a part of a general or localized peritonitis, or as a result 




Fig. 201.— Malarial Spleen. 

Showing thickening of the trabec- 
ular network of the pulp, with pig- 
mentation of the pulp cells. 



THE SPLEEN AND THYMUS. 379 

of lesions of the spleen itself, such as infarctions, abscesses, and acute 
hyi)erplastic inflammation. Under these conditions a fibrinous pellicle, 
with more or less pus, may be formed on the surface of the organ. 
Chronic Inflammation, resulting in the production of new connective 
tissue, either in x^atches or as a more or less general thickening of the 
capsule, is of frequent occurrence. It may follow acute inflammation of 
the capsule, or be a part of general or localized chronic peritonitis. It 
is common in connection with chronic indurative splenitis, and it may 
occur from unknown causes. Sometimes the capsule is three or four 
millimeters in thickness over a considerable area ; sometimes very small 
nodular thickenings or papillary i:)rojections occur. As a result of this 
process adhesions, sometimes very extensive, may form between the 
sj)leen and adjacent parts. The thickened capsule is sometimes more 
or less extensively calcified. 



CHRONIC ENDOTHELIAL HYPERPLASIA OF THE SPLEEN. 

("Primary Splenomegaly.") 

Bovaird has recently described a slowly progressive lesion developing 
in early life in which the si^leen was greatly enlarged and firm in text- 

m . ■" - '* ■"..,'-■ ' ' - •<»■ .*, -" ' 



m- 



t 



''^^^A.- s> 



Fig. 202.— Chronic Endothelial Hyperplasia op the Spleen. 
Showing increase in number and exfoliation of the endothelium of the cavernous veins. 

ure, presenting on section numerous irregular white or yellowish areas, 
extending from the cai)sule into the substance of the organ. The splenic 
and mesenteric lymph-nodes and the liver were enlarged. On microscopic 
examination the spleen lesion was found to consist largely of an excessive 
proliferation of the endothelial cells of the pulp (Fig. 202), in part alone, 
in iDart associated with fibrous hyperplasia. Similar endothelial hyper- 
plasia occurred in the splenic and mesenteric lymph-nodes and in the 
connective tissue of the liver. There was marked pigmentation of the 



380 THE SPLEEN AND THYMUS. 

involved lymph -nodes and in the liver lesion. This condition has ap- 
parently been several times described, but has been usually regarded as 
tumor rather than endothelial hyperplasia. ' 



ALTERATIONS OF THE SPLEEN IN LEUKiEMIA AND PSEUDO- 

LEUKiEMIA. 

The lesions of the spleen are essentially similar in both of these con- 
ditions. They consist, in general, of an hyperplasia, sometimes most 
marked in one, sometimes in another of the structural elements of the 
organ, but they usually all participate in the alterations. The changes 
which occur in the earlier stages are but little known. The gross ap- 
pearances of the spleen vary. It is as a ru]e enlarged and sometimes is 
ten or fifteen times the normal size. It is commonly hard, but is some- 
times of the ordinary consistence, or softer, and the capsule is gener- 
ally thickened and rough. The section of the spleen may be of a uni- 
form dark- red color, but it is more frequently mottled red and gray. 
Sometimes the glomeruli are inconspicuous, but they are very often 
enlarged and prominent. They may be two to four mm. in diameter, 
and, owing to an infiltration of the arterial sheaths with lymph cells, 
may appear to the naked eye as grayish, round or elongated bodies, 
arranged along branching, interrupted, grayish streaks. The trabeculoe 
may be greatly thickened, as also the reticulum of the pulj), so as to be 
evident to the naked eye. Brown or black pigment may be collected 
around the glomeruli or in the pulp. Hsemorrhagic infarctions or cir- 
cumscribed extravasations of blood may further complicate the picture. 

Microscopically the api)earances are essentially the same as those 
above described in acute hyperplasia and in chronic interstitial splenitis, 
depending upon the stage and variety of the disease. Owing to the great 
size which some of such spleens attain they are liable to displacement, and 
they may interfere by pressure with the functions of neighboring organs. 

TUMORS. 

Primary tumors of the spleen are rare. Small fibromata, sarcomata, 
and cavernous angiomata sometimes occur. Sarcoma and carcinoma may 
occur in the spleen secondarily either as metastatic tumors or by exten- 
sion from some adjacent part, as the stomach. Dermoid cysts are de- 
scribed, but are rare. Other larger and smaller cysts, whose mode of 
origin is in most cases obscure, not infrequently occur. 

PARASITES. 

Pentastomum denticulatum is not infrequently found in the spleen, 
usually encapsulated and calcified. Cysticercus is rare. Echinococcus is 

^ For details of this lesion, with bibliography, see Bovaird, American Journal of the 
Medical Sciences, vol. cxx., p. 377, 1900. 



THE SPLEEN AND THYMUS. 381 

occasionally found, and, if tlie cysts are large or numerous, may cause 
more or less extensive atrophy of the organ. 

Various forms of bacteria have been found in the spleen. The pyo- 
genic cocci have been found in pyaemia, small -pox, ulcerative endocardi- 
tis, diphtheria, and under other conditions. The Bacillus anthracis oc- 
curs here in anthrax ; the Bacillus tuberculosis in tuberculous inflammation ; 
and typhoid bacilli in typhoid fever. Spirochsete Obermeieri may be pres- 
ent in relapsing fever. 

The Thymus. 

MALFORMATION AND HYPERTROPHY. 

Small accessory thymus gljands are occasionally found near the th5^roid. 

It is usual for the development of the thymus to reach its height in the early years 
of hfe. It then undergoes involution or atrophy, losing its epithelial characters and 
becoming largely composed of lymphoid cells. It is finally represented in old age by a 
small mass of fat tissue. Occasionally, however, the thj-mus persists until youth or 
middle age. ^ Furthermore, it may become enlarged — so-called hypertrophy of the thy mus. 
The enlargement is, however, due to an hyperplasia rather than hypertrophy : the new- 
formed tissue ma}' present a more or less marked lobulated or glandular appearance. 
This new- formed tissue, according to the studies of Sultan and Lochte, may be largely 
composed of lymphoid cells, or of larger polyhedral cells, so-called "epithelioid " cells.^ 



HiEMORRHAGE. 

Small, and sometimes large, hsemorrhages are occasionally seen in the 
thymus of young children as the result of venous congestion in asphyxia, 
poisoning, etc. They may also occur in the hgemorrhagic diathesis. 



INFLAMMATION. 

Suppurative inflammation of the thymus is of occasional occurrence, 
and is usually secondary to a similar inflammatory process in some other 
part of the body. Tuberculous and syphilitic lesions of the thymus are 
described, but are rare. 

TUMORS. 

Sarcoma is the most common tumor ; Endotheliomata and Dermoid Tu- 
mors are recorded. 

' For the significance of a persistent thymus in certain cases of sudden death, see 
J^orton, Phila. Med. Jour., vol. i., p. 249, 1898, bibl. On the relationship of hyper- 
plasia in a persistent thymus to Hodgkin's disease, consult Brigidi and Piccoli, Ziegler's 
Beitr. z. path. Anat.. etc., Bd. xvi., p. 388. 

■^See Lochte, Centb. f. allg. Path. u. path. Anat., Bd. x., p. 1, bibl. 



CHAPTER IV. 

THE THYROID AND ADRENALS. 
The Thyroid. 

Malformations. 

The thyroid gland is sometimes veiy small, either as the result of atrophy (Fig. 
203) or as a congenital deticiency. For the relationship of this condition to cretinism 
and myxoedema see page 331. 







ISK 


^<Il' 

^'^ 










!»': 




































\^), -■- = :- 




',■•:.' ". ■ 1 •'[ ,' ■'■ 








.'>.l^r'' 









Fig. 203.— Section of the Atrophied Thyroid Gland in Myxedema. 
a, Interstitial tissue ; 7j, atrophied lobules with small spheroidal-celled or lymphatic tissue in their peripheries. 

The thyroid may be irregularly lobulated. There may be small accessory glands 
situated at some distance from the normal position, as in the mediastinum or pleura. 



DEGENERATION. 

Colloid degeneration of the epithelial cells of the gland, aucl the filling 
of the alveoli with colloid material, are of common occurrence, and when 
in moderate degree may be regarded as normal, since a certain amount of 
this change is found in many otherwise apparently normal glands. It 
may occur, however, to such an extent as to constitute an important 
lesion (see below). 

Amyloid degeneration, particularly of the blood-vessels, is of infrequent 
occurrence. 

Hyalin degeneration of the stroma of the thyroid may occur. 



THE THYROID AND ADRENALS. 383^ 



DISTURBANCES OF CIRCULATION. 

Hypergemia of the thyroid giand, often accompanied by considerable 
enlargement of the organ, may be the resnlt of valvnlar disease of the 
heart ; it occnrs in Basedow's disease ; it may be temporary or perma- 
nent, and in the latter case may be associated with the formation of new 
connective tissue. Hsemorrhages may occur, leading to pigmentation of 
the organ. 

INFLAMMATION. (Strumitis.)^ 

Inflammation of the thyroid gland is not very common and may occur 
under a variety of conditions. It may result in the formation of larger 
and smaller abscesses or in the production of new connective tissue which 
may be associated with atrophy of the parenchyma. Tuberculous inflam- 
mation, with the formation of miliary tubercles, is of infrequent occur- 
rence. ' Syphilitic inflammation, with the formation of gummata, has been 
described, but is rare. ^ ^^ 

STRUMA. (Hyperplasia of the Thyroid; Goitre.) "^ * 

Among the most important of the lesions of the thyroid is the 
enlargement of the organ commonly known as the goitre or struma. The 
enlargement of the gland may occur in several ways. Thus, a simple 
hypergemia may, as above stated, lead to considerable enlargement of 
the organ, and this is sometimes called struma liyxjercemica. The true goi- 
tre, however , consists in the enlargement of the old and the formation 
of new gland alveoli, while with these changes there is very frequently 
associated a greater or less amount of colloid degeneration. When there 
is new formation of gland tissue the growth has the character of an ade- 
noma. The hyperplasia may occur diffusely, so that the whole gland is 
more or less enlarged ; or it may occur in the form of circumscribed nod- 
ules. When the colloid degeneration is prominent, so that the tumor 
has a gelatinous appearance, it is called colloid struma (Fig. 204).^ Ac- 
cumulations of fluid, blood, colloid, etc., in the old or new-formed alveoli, 
may lead to dilatation and atrophy of the walls of the alveoli, so that 
cysts, sometimes of large size, are formed. Thus occurs the cystic struma. 
Again, the blood-vessels may undergo marked dilatation, so that we may 
have a telangiectatic struma^- or, cavernous angiomata may form within 
goitres. Yery frequently all these varieties of lesions are present in the 
same goitre. The appearances may be rendered still more complex by 
the occurrence of haemorrhages and pigmentation, calcification, purulent 

^ See Boger and Gamier, Arch. gen. de Med., t. iii., p. 385, 1900, bibl. 

■^For a stud)^ of the normal and pathologic histology of the thyroid, with biblio- 
graphy, consult MiUIer, Ziegler's Beitr. z. path. Anat., etc., Bd. xix.,''p. 127. 1896. For 
myxoedema and Basedow 's'disease, see pp. 331 and 332. 

^ For a consideration of the nature of colloid and its formation in struma see Bein 
bach, Ziegler's Beitr. z. path. Anat., etc., Bd. xvi., p. 596, bibl. 



384 



THE THYROID AND ADRENALS. 



or indurative inflammation (strumitis), and by the not very infrequent 
association with carcinoma and sarcoma. The excitants of goitre are not 
well understood. The growth is, as a rule, slow, but occasionally a very 
rapid enlargement occurs as the result of a sudden increase of the col- 
loid degeneration. In many cases even very large goitres give rise to 
but moderate inconvenience, but they may assume great significance by 







Fig. 204.— Colloii? Struma— Goitre. 
The colloid material filling the alveoli is stained red. 



encroaching upon neighboring parts. Thus death may be caused by 
pressure on the trachea, oesophagus, or on the large vessels. 



TUMORS. 



Some of the forms of goitre above described may be regarded as 
tumors or may be associated with tumors. Sarcoma and endothelioma are 
the most common tumors of the thyroid. 

Sarcoma, either spheroidal or spindle -celled, may occur as primary 
tumors in the thyroid, either in otherwise normal glands or in connec- 
tion with struma. ' Melano-sarcoma has been observed. Secondary sar- 
comata are rare. 

Primary carcinoma, both glandular and scirrhous, occurs in the thy- 
roid, and, particularly in the softer forms, may spread to adjacent parts 
and occasionally form distant metastases. Dermoid cysts are of occa- 
sional occurrence. 

1 Consult for summary of observations on sarcoma of the thyroid, Morf, Jour, A.m. 
Med. Ass'n, April 29, 1899, bibl. 



THE THYKOID AND ADEEXALS. 385 

PARASITES. 
Echinococcus cysts have been found in the thyroid. 

The Adrenals (Suprarenal Bodies, Suprarenal Capsules). 

Malf ormatioiis . 

In acephalic and other monsters the adrenals may be atrophied or entirely ab- 
sent. Sometimes in well-formed adults these organs cannot be discovered. There 
may be little rounded nodules loosely attached to the surface of the adrenals and hav- 
ing the same structure. Accessory and misplaced adrenals are not uncommon. A few 
cases have been reported of accessory adrenals in the broad ligament.' They may be 
present in the liver. ^ 

If one kidney be absent or in an abnormal position its adrenal usually retains its 
proper position.^ 

ATROPHY AND DEGENERATION. 

Atrophy of the adrenals may be extreme. 

Fatty degeneration of the cortical portion is the rnle in the adult. It 
sometimes occurs in nodular areas. In children under five years of age 
it is pathological. 

Amyloid degeneration may involve both the cortical and medullary 
portions. In the cortex it usually involves only the walls of the blood- 
vessels ; in the medulla both the blood-vessels and the cells of the paren- 
chyma may undergo this degeneration. The organs are usually firm 
and have a grayish, semi-translucent appearance. 

Pigmentation of the inner cortical zone is frequent in old jpersons. 

THROMBOSIS AND HAEMORRHAGE. 

Venous and capillary thrombosis may occur. 

In children, soon after birth, it is not very infrequent to find large 
haemorrhages in one of the adrenals, converting it into a cyst filled with 
blood. This lesion has been observed in a few cases in adults. ' 

INFLAMMATION. 

Suppurative inflammation, with the formation of abscesses, has been 
seen in a few cases. 

The most frequent lesion of the adrenals is tuberculous inflammation. 
They are usually increased in size ; their surfaces are smooth or nodular. 

^ See Warthin, American Journal of Obstetrics, vol. xlii., 1900, bibl. 
•2 See Myes, Trans. New York Path. Soc, 1899-1900. 

^For consideration of relationship of the adrenals to the nervous system, see Ale.v- 
ander, Ziegler's Beitr. z. path. Anat., Bd. xi., p. 145, bibl. 

'^For bibliography see Arnaud, Arch. gen. de Med., t. iv., p. 5, 1900. 
25 



386 THE THYROID AND ADREN^ALS. 

The normal structure of the gland is more or less replaced by tubercle 
tissue, which usually undergoes cheesy degeneration and may soften. 
Fibrous tissue may form in considerable amount. (See Addison's Dis- 
ease, page 332. ) 

Syphilitic infiammation, with and without the development of gum- 
mata, is of occasional occurrence. 



TUMORS. 

Sarcoma, glioma, and endothelioma occur in the adrenals. 

Neuroma. — Ganglionic neuromata have been described by Weichsel- 
baum and Freeman. 

Hyperplasia of the gland tissue (adenoma or struma suprarenalis lipo- 
matosa), with fatty degeneration in the form of circumscribed nodules, is 
of occasional occurrence. 

Adenomata of the adrenals, resembling in type the structure of the 
cortex, may form as large vascular tumors, often hsemorrhagic, which 
may invade the neighboring vessels and form metastases. Some of the 
so-called adenomata of the kidney are probably adenomata of displaced 
accessory adrenals. 

Carcinoma is not common, but may be primary or secondary. ^ 

^ For bibliography of primary malignant tumors of the adrenals, see Ramsay, Johns 
Hopkins Hospital Bulletin, vol. x., pp. 20, 1899. 



CHAPTER V. 

THE CIRCULATORY SYSTEM. 

The Pericardium. 

INJURIES. 

The pericardium, maybe injured by penetratiug weapons, by gunsliot 
wounds, and by fragments of bone. It may be ruptured by severe con- 
tusions of the thorax, and by rapid extravasation of blood into the peri- 
cardial sac. Perforations may occur with empyema, mediastinal abscesses, 
abscesses of the chest wall and of the liver, or in connection with aneur- 
isms of the aorta and suppurative inflammation of the pericardium. 

HAEMORRHAGE. 

Extravasations of blood into the cavity of the pericardium may fol- 
low wounds and rupture of the heart, mixture of the aorta and of aneur- 
isms, and may occur with pericarditis. Small extravasations in the 
substance of the pericardium are found with scurvy, purpura, and in 
infectious diseases. 

DROPSY. (Hydropericardium.) 

At autopsies a few hours after death a few cubic centimetres of clear, 
light-yellow serum are usually present in the pericardial sac. If decom- 
position have commenced, this may be reddish, or it may be slightly tur- 
bid from the falling-off of the pericardial endothelium. 

Large accumulations of clear yellowish serum are often found as part 
of general dro^Dsy from heart disease, kidney disease, etc. The amount 
is sometimes so great as to interfere with the movement and nutrition of 
the heart. 

PNEUMONATOSIS. 

Air or gas in the pericardium is sometimes present as the result of 
post-mortem decomposition and may be accompanied with drying of por- 
tions of the pericardium. Wounds or paracentesis of the pericardium ; 
the perforation of ulcers of the stomach, cavities of the lungs, and ulcers 
of the oesophagus, may admit air into the pericardial cavity. In puru- 
lent pericarditis with foul, decomposing exudate, gases may be evolved. 



388 



THE CIRCULATORY SYSTEM. 



INFLAMMATION. (Pericarditis.) 

Pericarditis is rarely primary ; but is usually secondary to infectious 
diseases, such as pneumonia, pleurisy, tuberculosis, typhoid fever, endo- 
carditis, and pyaemia. It may follow injuries and is frequently associ- 




Fig. 205.— Fibrinous Pericarditis. 
The pericardial sac is laid open and the heart is seen covered with an irregular villous layer of fibrin. 

ated with rheumatism or inflammation of the kidneys. It may be exu- 
dative or productive in character. 

Exudative Pericarditis. — It is convenient to distinguish in exudative 
pericarditis Si fibrinous, a sero -fibrinous, and ^ purident form. 

Fibrinous and Seko- fibrinous Pericarditis. — In the earlier 
stages or lighter forms of fibrinous pericarditis, the whole surface or 
portions of the pericardium may be dull or slightly roughened from a 
delicate fibrinous pellicle, more or less hypersemic and often studded with 
minute petechise. Later, if the exudate accumulate, the entire surface 
of the pericardium may be covered with a net-like layer of thick masses 
of fibrin. This may cover both the visceral and parietal surfaces and 
is often beset with irregular villosities (Fig. 205). Fibrinous adhesions 
may form between the two layers. There is usually some serous fluid 
as well as leucocytes mingled with the fibrin. 



THE CIBCULATOEY SYSTEM. 389 

Serum may accumulate in considerable quantity — sero -fibrinous j[)eri- 
carditis. The pericardial sac may be greatly distended with this form of 
exudate so as to displace the heart and compress the larger air passages, 
the oesophagus, or the aorta. 

Purulent Peeicaeditis. — In this form of exudative pericarditis 
there are usually more or less serum and fibrin mingled with pus cells and 
often red blood cells. The process may start as a sero -fibrinous inflam- 
mation. It is apt to occur as an extension of an infectious process in the 
neighborhood or as a part of a general pysemic process. Streptococcus 
pyogenes, micrococcus lanceolatus, staphylococcus pyogenes aureus, and 
the tubercle bacillus are the bacteria most commonly found in exudative 
pericarditis. 

Chronic Pericarditis.^In exudative pericarditis the mesothelium^ (en- 
dothelium) in the early stages, and later this with the underlying connec- 
tive-tissue cells, contribute to the cellular elements in the exudate. In 
recover}^ the exudates degenerate and are gradually absorbed, while from 
the blood-vessels and the connective-tissue cells of the pericardium more 
or less new fibrous tissue is formed, at first very cellular and vascular, 
later dense in character. There may finally be local or general thicken- 









^'\ 



Fig. 206.— Obliteration of the Pericardial Sac i\ a Child, Following Pericarditis. 

Showing blood-vessels growing from the visceral pericardium into the blood clot filling the sac. Trans- 
verse section. A, Heart ; B, pericardium ; C, new-formed vascular tissue extending above to the unorgan- 
ized clot. A similar layer of new vascular tissue was present over the parietal pericardium, and in places 
the two layers had coalesced, obliterating the sac. 

ings of the pericardium or adhesions between the visceral and parietal 
layers. The new fibrous tissvie may extend between the subi^ericardial 
muscle fibres of the heart. Calcification of this new-formed fibrous tissue 
may occur. 

Obliteration of the Pericardial Sac. — As the result of the for- 

^ See reference to Minot, p. 295. 



390 THE CIRCULATORY SYSTEM. 

mation of vascular new connective tissue between the pericardial walls, 
the sac may be partially or wholly obliterated (Fig. 206). 

This may be the conclusion of an acute inflammatory process or it 
may result from the organization of a blood clot following haemorrhage 
into the sac. It may occur as the result of the latter process early in life. 

Supra- Aeteeial Epicardial Fibroid Nodules. — Small fibrous 
nodules are occasionally formed along the branches of the coronary arte- 
ries, especially on the surface of the ventricles. According to the studies 
of Knox' they are frequently associated with lesions of the arteries, lead- 
ing to the weakening of their walls at these situations. 

Tuberculous Pericarditis. — This lesion may occur by itself, but is apt 
to be associated with other tuberculous inflammation in the vicinity of 
the heart. There may be miliary tubercles scattered diffusely, or limited 
to certain regions in the pericardium, which is otherwise little changed. 
Kot infrequently, however, there is a considerable thickening of the peri- 
cardium, either visceral or parietal, or both. 

In such cases the new -formed tissue consists of fibrous tissue and of 
tubercle tissue which has undergone extensive cheesy degeneration. The 
thickened visceral and parietal layers of the pericardium are often more 
or less grown together, so that the pericardial sac may be partially or 
almost completely obliterated. An inflammatory exudate often accom- 
panies the tuberculous process. 

TUMORS. 

Fibromata are sometimes developed in the pericardium. They are 
often of polypoid form, and from atrophy of the pedicle may become free 
in the pericardial sac. Endotheliomata are of occasional occurrence as 
primary tumors. 

Sarcomata and carcinomata occur as secondary growths either from 
continuous infiltration or as metastatic tumors. Primary sarcoma of the 
pericardium has been described. "" 

Cysts of the visceral pericardium have been described. We have seen 
a peclniTculated cyst, containing about 6 c.c. of clear fluid, hanging into 
the pericardial sac from its attachment near the pulmonary artery. The 
origin of such cysts is obscure. 

The Heart. 

Malformations and Malpositions. 

Malformations op the Heart. — The malformations of the heart are usually 
closely associated with malformations of the aorta and pulmonary artery. They de- 
pend on arrest of, or abnormal, development ; on endocarditis, myocarditis, thrombosis, 
or mechanical causes. 

I. The common arterial trunk is only partially, or not at all, separated into aorta 
and pulmonary artery. The divisions between the heart cavities are at the same time 

^ Knox, Journal of Experimental Medicine, vol. iv., p. 245, 1899. 
"^Williams, New York Med. Jour., April 14th, 1900, bibl. 



THE CIRCULATORY SYSTEM. 



391 



defective, so that there may be one ventricle and no auricles ; one ventricle and one 
auricle — reptilian heart ; or one ventricle and two auricles. 

II. The trunk of the pulmonary artery or of the aorta is stenosed or obliterated, 
and from the obstruction to the current of blood there is interference with the develop- 
ment of the septa between the heart cavities. 

1. The aorta, at its origin, or in the ascending portion of the arch, is stenosed or 
closed. The pulmonary artery gives ofl" the descending aorta, and supplies the carotids 
and subclavians. The foramen ovale remains open, or there is no septum between the 
auricles. The ventricular vseptum is also usually defective. The right ventricle is 
hypertrophied. 

2. The pulmonary artery is stenosed or closed. Its branches are supplied by the 




Fig. 207.— Opening in the Ventricular Septum of the Heart— Interventricular Foramen. 
The opening is about 5 mm. in diameter, and its edges are formed by fibrous tissue. 



aorta, through the ductus arteriosus. The ventricular septum is defective, the foramen 
ovale is open, or the auricular septum defective. 

III. The malformation affects the aorta and pulmonary artery after they are more 
fully developed. 

1. There is stenosis of the aorta between the left subclavian and ductus arteriosus, 
or just at the opening of the ductus arteriosus. The descending aorta is then a con- 
tinuation of the pulmonary artery. 

2. The aorta gives off all its branches from the arch, but the descending aorta is a 
continuation of the pulmonary artery ; or the carotids may spring from the aorta, the 
subclavians from the pulmonary arter3\ 

3. The vessels are transposed; the pulmonary artery arises from the left, the aorta 



392 THE CIRCULATORY SYSTEM. 

from the right ventricle ; the pulmonary veins empty into the left, the venae cavse into 
the right auricle; or the veins also may be transposed. The septa are defective. 

IV. The aorta and pulmonary artery are normal, but the cardiac septa are defective. 

1. The foramen ovale remains partl}^ open. This condition may continue through 
life without ill effects. It has been found by some observers in about one-fifth of their 
autopsies. 

2. The ductus arteriosus may remain open for many years; this also may cause no 
disturbance. 

3. There is a small or large opening in the ventricular septum, usually in its upper 
part (Fig. 207). This may give rise to no symptoms, unless disease of the heart or 
lungs be superadded. 

Y. Either of the auriculo-ventricular orifices may be entirel}^ closed. The fora- 
men ovale remains open, and the ventricular septum is defective. ^ 

VI. The valves of the different orifices of the heart may be absent or defective. 
The arteries or the ventricles are usually defective at the same time. 

The aortic and pulmonary valves may consist of two large or four small leaves. 




Fig, 208.— Eenestration of the Semilunar Valves. 

instead of the usual three. The edges of the semilunar valves ma}' be fenestrated 
(Fig. 208). These alterations are usually of no significance. 

Generally speaking, the existence of openings between the two auricles or the two 
ventricles, admitting some admixture of venous and arterial blood, produces no marked 
change in the circulation. If, however, the passage of the current of venous blood into 
the right heart is in any way interfered with, the consequences are very serious. Cyan- 
osis is produced, the skin is of a bluish color, the small veins and capillaries are dilated, 
exudation of serum and hypertrophy of connective tissue take place, especially in the 
fingers and toes. 

Besides the malformations already mentioned we mayfind : entire absence of theheart ; 
abnormal septa and chordae tendineae in the heart cavities ; abnormal shapes of the heart. 

Very rarelj^ two more or less perfect hearts are found in the same thorax. 

Malpositions of the Heart. — (1) There is a smaller or larger defect in the walls 
of the thorax, so that the heart projects on the outside of the chest; the pericardium is 
usually absent. 

(2) The diaphragm is absent, and the heart is in the abdominal cavity. 

(3) The heart is in some part of the neck or head; this occurs only in foetuses very 
much malformed. 

^ Consult for a study of rare forms of cardiac anomalies, HeMoen, Am. Jour. Med. 
Sciences, vol. cxxi., p. 163, 1901, bibl. 



THE CIECULATOIiY SYSTEM. 393 

(4) The heart is transposed, being on the right side. 

Abnormal Size of the Heart. — (1) The heart may be abnormally large in con- 
nection with obstructive anomalies of the great vessels. 

(2) The heart may be abnormally small (hypoplasia). This abnormality is apt to 
be associated with the so-called status lymphaticus (see page 337). 

Displacements op the Heart. — Changes in the position of the heart are con- 
genital or acquired. The congenital malpositions have already been mentioned. 

The acquired malpositions maj^ be associated with : 

1. Hypertrophy of the heart ; its long axis approaching the horizontal position. 

2. Changes in the thoracic viscera. Emphysema of both lungs maj^ push the heart 
downward. Emphysema, pleurisy with effusion, or pneumothorax of one side pushes 
the heart to the other side. Pleurisy or chronic pneumonia, producing retraction of one 
side of the thorax, draws the heart to that side. New growths, aneurisms, and curva- 
tures of the spine displace the heart in various directions. 

3. Changes in the abdomen. Accumulations of fluid and new growths in the ab- 
domen, and tympanites, may push the heart upward. 



WOUNDS AND RUPTURES. 

Wounds of the heart are most frequently made by penetrating instru- 
ments, by bullets, and by fragments of bone. The right ventricle is the 
more frequently wounded; next the left; rarely the auricles. The 
wound may penetrate into the cavities of the heart or pass only partly 
through its wall, or a bullet or the broken end of a weapon may be em- 
bedded in the wall. If the wound penetrate a cavity and be gaping, 
death may follow instantly and the pericardium be found filled with 
blood. If the wound be small and oblique, the blood may escape grad- 
ually and death may not ensue for several days. In rare cases adhesions 
are formed with the pericardium and the wound cicatrizes. Wounds 
which do not penetrate may cause death by the inflammation which they 
excite, or they may cicatrize. 

Bullets and foreign bodies may become encapsulated in the heart wall 
and remain so for years. 

Rupture of the heart wall occurs in various ways : 

1. Severe contusions of the thorax may produce rupture, usually of 
one of the auricles. ^ 

2. Spontaneous rupture occurs usually in advanced life. Eui3ture 
is most frequent in the left ventricle, and, in a considerable proportion of 
cases, near the apex. There is usually one rupture, but sometimes there 
are more. The rupture is usually oblique and larger internally than ex- 
ternally. The heart wall, near the seat of rupture, may be infiltrated with 
blood, or blood may infiltrate the subpericardial fat. The heart wall 
may be of normal thickness, or thin ; it is usually soft and in a condition 
of fatty infiltration or degeneration. The rupture very frequently takes 
place when the iDatient is quiet. Death may be almost instantaneous or 
may not ensue for several hours. 

Fatty degeneration leading to rupture of the heart may be general, or 
it is frequently circumscribed and due to obliterating endarteritis, athe- 

'For bibliography see Newton, Med. Record, June 17th, 1899. 



394 



THE CIRCULATORY SYSTEM. 



roma, thrombosis, or embolus of one of the coronary arteries, whereby a 
portion of the heart wall is deprived of nourishment and degenerates. Or 
rupture of a branch of one of the coronary arteries may induce rupture 
of the heart wall. Acute and chronic myocarditis, with or without the 
formation of abscess or cardiac aneurism, or the presence of tumors in the 
heart wall, or hydatids, may lead to rupture. ' 

3. In rare cases rupture is associated with stenosis of the aorta and 
dilatation of the heart cavities. 

4. Eupture of the papillary muscles and tendons may be due to fatty 
degeneration or inflammatory or ulcerative processes. 



ATROPHY. 

Atrophy of the walls of the heart may be accompanied with no change 
in the size of its cavities; or with dilatation ('^passive dilatation ^^) ; or, 

more frequently, with diminution 
in the size of the cavities. 

The atrophy involves most 
frequently all the cavities of the 
heart, but may be confined to one 
or more of them. 

The muscular tissue appears 
normal, or may be brown from the 
presence of little granules of pig- 
ment in the muscle fibres, which 
are sometimes present in large 
numbers — hrown atrophy -, or the 
muscle fibres may undergo fatty 
degeneration ; or there may be an 
abnormal accumulation of fat 
beneath the pericardium ; or there 
may be a peculiar gelatinous 
material beneath the pericardium 
— this consists of fat which has undergone mucous degeneration. The 
heart may be so much atrophied as to weigh only four ounces. 

Atrophy of the heart may be congenital ; it may be associated with 
repeated hsemorrhages or wasting diseases, or senility, with chronic peri- 
carditis, with effusion, with obstructive lesions of the coronary arteries, 
with chronic myocarditis, or mitral stenosis. 

Atrophy of the Pericardial Fat Tissue not infrequently occurs in per- 
sons emaciated by chronic disease, and then the usual situations of the 
fat are occupied by a tissue resembling mucous tissue in its gross charac- 
ters. Microscopical examination shows that in this atrophic fat the fat 
cells have largely lost their contents, and the whole tissue has undergone 
a partial reversion to its embryonic form (see Fig. 209). 




Fig. 309.— Atrophic Pericardial Fat Tissue. 

From a young person dead of carcinoma of the stom- 
ach and peritoneum. Stained with osmic acid and 
teased. 



* Consult Councilman, "On Sudden Deaths due to the Heart." 
Surg. Journal, November 9th, 1893. 



Boston Med. and 



THE CIKCULATORY SYSTEM. 395 



HYPERTROPHY. 

Hypertrophy may involve the walls of one or more or all the cavities 
of the heart. While the wall of a ventricle is thickened, its cavity may 
retain its normal size — simple hypertrophy ; or be dilated — excentric hyper- 
trophy ; or it may be contracted — concentric hypertrophy. 

Care should always be exercised in judging of this condition, for a 
firmly contracted heart seems to have a small cavity and thick walls. 
The existence of such a condition as concentric hypertrophy is denied by 
some authors. Excentric hypertrophy is the most common form. Sim- 
ple hypertrophy is not common, but may occur in connection with the 
atrophied kidneys of chronic diffuse nephritis. The muscle tissue in 
hypertrophied hearts is firmer and denser than normal, and is apt to have 
a darker color. Fatty degeneration may, however, be associated with 
it, giving the walls a lighter appearance. It is probable that the increase 
of tissue in the hypertrophied heart wall is the result of increase both in 
size and number of the muscle fibres. ^ 

Hypertrophy of both ventricles increases both the length and breadth 
of the heart. Hypertrophy of the left ventricle (alone) increases its 
length. The apex is then lower and farther to the left than usual. Hy- 
]3ertrophy of the right ventricle (alone) increases the breadth of the 
heart toward the right side ; but sometimes the right edge of the heart 
retains its normal situation and the apex is displaced to the left. With 
large hypertrophy of both ventricles, the base of the heart may sink, so 
that its long axis approaches a horizontal direction. 

Hypertrophied hearts may weigh from forty to fifty ounces, or even 
more. 

Hypertrophy of the heart may depend upon a variety of conditions 
which increase its work. 

1. Changes in the valves; either insufficiency or stenosis in the 
valves leading from a cavity, and insufficiency in valves leading to a 
cavity, may induce hypertrophy of its walls. 

2. Obstruction to the passage of blood through the arterial system, 
as in arterio- sclerosis and other lesions of the arteries; congenital or 
acquired stenosis of the aorta or other vessels, pressure of tumors, etc. , 
on vessels. Certain forms of chronic diffuse nephritis, especially atro- 
phied kidneys, lead to hypertrophy of the left ventricle, and sometimes 
secondarily to hypertrophy of the right ventricle. 

3. Obstruction to the passage of blood through the pulmonary artery 
by stenosis or by certain diseases of the lungs, particularly emphysema 
and chronic phthisis, may lead to hypertrophy of the right ventricle, 
and, secondarily, of the right auricle and left ventricle. 

4. Any cause, whether muscular or nervous, which increases the ra- 
pidity and force of the heart's contractions, may induce hypertrophy. 

_ ^ For a suggestive study of cardiac hypertrophy see Welch, " Adaptation in Patho- 
logical Processes." Trans. Congr. of American Physicians and Surgeons, vol. iv., 1897. 



396 THE CIRCULATORY SYSTEM. 

5. Dilatation of the ventricles, from any cause, is frequently followed 
by hypertrophy. 

6. Pericarditis may lead to hypertrophy by induciug softening and 
dilatation of the ventricles, or by leaving adhesions which obstruct the 
heart's action. Chronic myocarditis also may lead to hypertrophy. 

Finally, for some cases of hypertrophy no satisfactory cause can be 
found. ' 

It should be borne in mind that an increase in the amount of fat in 
and about the heart may make the organ appear larger, when there may 
be actually a considerable decrease in the amount of muscle tissue. 

DILATATION. 

Dilatation may be combined with hypertrophy — active dilatation / or 
there may be no increase of muscle tissue, but a thinning of the walls 
proportionate to the dilatation of the cavity — passive dilatation. 

Either one or all of the heart cavities may be dilated, the auricles 
most frequently ; next the right ventricle ; least often the left ventricle. 

Active dilatation has been considered under hypertrophy. 

Passive dilatation may be associated with : 

1. Changes in the valves. Mitral or aortic stenosis or insufficiency 
may lead to dilatation of the auricles and right ventricle. Pulmonary 
stenosis or insufficiency may lead to dilatation of the right auricle and 
right ventricle. Aortic insufficiency, with or without stenosis or mitral 
insufficiency, may lead to dilatation of the left ventricle. Dilatations 
under these conditions are often succeeded and compensated for by 
hypertrophy of the heart walls. 

2. Changes in the muscle tissue of the heart walls. Serous infiltra- 
tion from pericarditis, myocarditis, fatty degeneration and infiltration, 
atrophy of the muscle fibres, may all lead to dilatation. 

3. A heart which is already hypertrophied may, from degeneration 
of the muscle, become dilated. 

4. Acute exudative inflammations of the lungs and acute pleuritic 
exudations, by rendering a large number of vessels suddenly imperme- 
able to the blood current, may produce sudden stasis in the pulmonary 
artery and dilatation of the right heart. 

5. There are curious and often serious cases of acute and chronic 
dilatation of the ventricles for which no mechanical explanation is found. 

CHANGES IN THE HEART VALVES. 

Fenestration of the valves is usually a change of no practical impor- 
tance. It occurs very frequently in the aortic and pulmonary valves. The 
valves may be thinner than usual, and close to their free edges are small 
slits extending from the centre to the attached edges of a leaf (Fig. 208). 

^ Howard's table of 105 cases of cardiac hypertrophy shows its association with 
arterio-sclerosis in 59 per cent; with nephritis in 13.4 per cent; with valvular lesion in 
12.4 per cent. Johns Hopkins Hospital Reports, vol. iii., p. 265. 



THE CIRCULATORY SYSTEX. 



397 



Aneurisms of the valves are formed iu two ways : 

1. They are the result of endocarditis. One of the lamellae of the 
leaf of a valve is destroyed, and the other lamella is converted into a sac 
filled with blood. These aneurisms are found in the aortic valve, pro- 
jecting into the ventricle ; and in the mitral valve, projecting into the 
auricle. Xot infrequently the wall of the aneurism gives way, so that 
there is a rupture entirely through the valve. 

2. The entire thickness of a leaf of a valve is iDOuched, forming a sac 
filled with blood. • This occurs in the aortic, mitral, and tricuspid valves. 

Haemorrhage in the substance of the valves is sometimes found in very 
young children. 

ANEURISM OF THE HEART. 

Sacs filled with blood, situated in the walls of the heart and communi- 
cating with its cavities, are formed in several different ways. 

1. In interstitial myocarditis a small or large portion of the wall may 
be replaced by fibrous tissue, and this yielding to the pressure of the 
blood from within, may be pressed outward. Such a pouch may be a 
circumscribed sae communicating with the heart cavity by a small open- 




FiG. 210.— Aneurism of the Heart Opening from the Left Ventricle into the Right auricle. 

Seen from behind. 



398 



THE CIRCULATORY SYSTEM. 



ing, or may be a simple dilatation of part of the ventricle. The wall of 
such an aneurism becomes thinner as the sac increases in size. It is com- 
posed of the endocardium, new fibrous tissue, visceral pericardium, and 
sometimes the adherent x)arietal pericardium. The walls may calcify, or 
rarely they become so thin as to rupture externally or into the right ven- 
tricle. The sacs may contain fluid blood or be filled with fibrin. 

Such aneurisms are usually situated in the wall of the left ventricle ; 
rarely in that of the left auricle. If they are in the septum they may 
project into the right ventricle or auricle (Fig. 210). They are usually 
single, but sometimes two or three are found in the same heart. 

2. Fatty degeneration of the heart wall may reach such a degree that 
the wall yields and is pouched out into an aneurismal sac. 

3. Endocarditis and myocarditis, or fatty degeneration, may so soften 
a portion of the heart wall that the endocardium and i^art of the muscu- 
lar tissue are ru^Dtured and a ragged cavity is formed. This form of an- 
eurism usually does not attain a large size, but soon ruptures externally 
and causes the death of the patient. 

Small aneurisms of the sinus of Valsalva are of occasional occurrence. 

THROMBOSIS OF THE HEART. 



It is common to find after death, in the heart cavities, yellow, succu- 
lent, semi-trausluceut masses. They are most common and of firmest 
texture in persons who die of acute inflammatory diseases. They may 

adhere quite firmly to the 
walls of the heart, and may 
extend in long, branching 
cords into the vessels. They 
are formed in the last hours 
of life and just after death. 
They hav€? no clinical or pa- 
thological importance. 

Coagula of the fibrin of the 
blood in the heart do, how- 
ever, form during life, and 
may exist for years. If the 
fibrin adheres to the valves in 
small masses these are called 
vegetations; if it coagulates 
in the heart ca^dties in larger 
bodies they are called thrombi 
or heart polypi. 

Such thrombi are found 
in all the heart cavities. 
They form flattened masses 

FIG. 311.-P0LYP0ID THROMBUS IN THE LEFT AURICLE OF ^^^\ adhcrCUt tO thC CUdO- 
THE JdLEART. ^ 

The thrombus was dark red in color, with smooth surface. Cardiuui ; Or rOUUded bodieS 




THE CIRCULATORY SYSTEM. 399 

in the spaces between the trabecnlse ; or have a polypoid shape and are 
attached by a narrow pedicle (Fig. 211), or very rarely are globular and 
free in the cavity of the auricle (Fig. 212). Cardiac thrombi are most 




Fig. 313.— Large Globular Thrombus in the Right Auricle op the Heart. 

frequent in the auricular appendages and between the columnse carnese 
near the apices of the ventricles. 

They are usually found in connection with some valvular lesion (Fig. 
213), which involves a roughening of the surface, or prevents the free 
circulation of blood through the heart. ' 

Old cardiac thrombi are firm, dry, and of a whitish color; they may 
soften and break down at their centres, so as to look like cysts filled 
with pus, or they may calcify. They are usually entirely unorganized, 
consisting simply of fibrin, but may become organized. 

Cases are reported of organized thrombi in the auricles, the seat of 
tuberculous inflammation. - 

^ For a study of cardiac thrombosis see Martin and Rennie, Lancet, 1899, ii., p. 782. 
See also Welch in Allbutt's "System of Medicine," vol. vi., p. 182. 

''Kotlar, Eef. Cbl. f. Bak., Abth. 1, Bd. xv., p. 498, 1894; also Moser, I. c, p. 406. 



400 THE CIRCULATORY SYSTEM. 

Sometimes sarcomatous and carcinomatous tumors in different parts 
of the body are accompanied by the formation of thrombi in the heart 




Fig. 213.— Thrombus Formed over the roughened Edge of the Mitral Valve. 

cavities, which are composed partly of coagulated blood, partly of tis- 
sue like that of the primary tumor. 

DEGENERATION. 

Albuminous Degeneration. (Parenchymatous Degeneration.) — This le- 
sion frequently occurs in diphtheria, ' typhoid and typhus fever, pyaemia, 
erysipelas, and other infectious diseases, as a result of burns, and under a 
variety of other conditions. It is characterized by the presence in the 
muscle fibres of the heart of greater or less numbers of albuminous gran- 
ules of various sizes, most of them very small. They are not as refractile 
as fat droplets, and are insoluble in ether, while swelling up and be- 
coming almost invisible under 
.;«•*:. the influence of acetic acid. 

Sometimes they are so abun- 
dant as to conceal the stria- 
tions of the fibres. The de- 
i;^^*^--; "^^SSr^S^ ; ^S'^- '^^ I generation is usually quite uni- 
y,1!i /'"-"^^^^^t^/^f..^^ formly diffused through the 

'f^^y^, . , 'i/^Lf^^fV?^'"J:w:Sfel heart, whose walls are softer 

than normal and of a grayish 
" ^ '*"^'of , ^JM^-yS^M^^^^'^" color. This lesion may be as- 

>,-,.-j/^^-^v.->i^ sociated with or followed by 

Fig. 214.— Fatty Degeneration of Heart Muscle. fatty degeneration. 

Fatty Degeneration of the 
Heart Muscle. — This consists in the transformation of portions of the mus- 
cle fibres of the heart into fat, ^ which collects in the fibres in larger and 
smaller droplets, sometimes few in number, sometimes so abundant as 

^ See reference, p. 236. ^ See in this connection, p. 80. 




THE CIRCULATORY SYSTEM. 401 

entirely to destroy or conceal the normal striations (Fig. 214). These 
droplets are soluble in ether, and remain unchanged on treatment with 
acetic acid. This degeneration is sometimes quite universal, but is more 
apt to occur in patches, giving the heart muscle a mottled appearance. 
This mottling may usually be best seen on the papillary muscles. The 
degenerated areas have a pale yellowish color, and the muscle tissue is 
soft and flabby ; but when moderate or slight in degree the gross appear- 
ance may be little changed, and the microscopical examination be neces- 
sary for its determination. This degeneration may lead to thinning of 




Fig. 215.— Fatty Infiltration of the Heart— Lipomatosis. 

The lesion is excessive, the heart muscle being to a large extent atrophied. (The fat cells are represented 
in the drawing, for the sake of clearness, of relatively too large size.) 

the walls, or to rupture of the heart, or to inability to fulfil its functions. 
It is not infrequently the cause of sudden death. 

Fatty degeneration may be secondary to hypertrophy of the heart, to 
inflammation of the heart muscle, or to pericarditis ; to disturbances of 
the circulation in the coronary arteries by inflammation, atheroma, etc. 
It may be due to deteriorated conditions of the blood in wasting diseases, 
excessive hsemorrhages, exhausting fevers, leukaemia, etc., to poisoning 
with phosphorus and arsenic, and to the toxins of microbic origin de- 
veloped in infectious diseases, such as diphtheria, scarlatina, typhoid 
fever, etc. ' It may occur in otherwise apparently healthy persons. 

Fatty Degeneration of the Endocardium. — It is not uncommon to find, 
especially in elderly persons, fatty degeneration occurring in patches, 
especially on the valves, but also on the general endocardium. It may 
also occur in ill-nourished and angemic individuals. Small, or even 
considerable, areas of fatty degeneration appear, as a rule, to be of lit- 
tle or no clinical significance. They are at least not inconsistent with 

^ Consult Flexner, Johns Hopkins Hospital Bulletin, vol. v., p. 26, 1894. 
26 



402 THE CIRCULATORY SYSTEM. 

perfect health. In these areas of fatty degeneration the connective- 
tissue cells are more or less completely filled T\dth larger and smaller fat 
droplets. 

Amyloid Degeneration of the endocardium or the walls of the blood- 
vessels and intermuscular connective-tissue septa is a not very infre- 
quent, but usually not very important lesion. 

Hyalin Degeneration sometimes occurs in the blood-vessels and in the 
muscle fibres. 

There may be calcification of the products of inflammation in pericar- 
ditis, or of connective-tissue membranes in chronic pericarditis ; in the 
latter case the heart may be more or less enclosed by a calcareous shell. 
The muscle fibres of the heart wall may, though rarely, become densely 
infiltrated with salts of lime. 

Fatty Infiltration. — This lesion, which should be clearly distinguished 
from fatty degeneration, consists of an unusual accumulation of fat 
about the heart and between its muscle fibres. 

The subpericardial fat, which may be present in considerable quantity 
under normal conditions, may be so greatly increased in amount as to 
form a thick envelope enclosing nearly the entire organ. Sometimes the 
accumulation of fat extends into the walls of the heart, between the 
mnscles, causing atrophy of the latter, frequently to a very great extent 
(Fig. 215), so that the function of the heart is seriously interfered with. 
This occurs sometimes in general obesity, or as a result of chronic peri- 
carditis, or in drunkards, or in debilitated or old persons. 



SEGMENTATION AND FRAGMENTATION OF THE MYOCARDIUM. 

Attention has been called by a number of observers to a condition of 
the heart muscle sometimes observed, it is said, in acute infectious dis- 
eases, in acute and chronic diseases of the central nervous system, and 
in sudden death from a variety of causes. The muscle tissue is soft, fri- 
able, opaque, and often yellowish. Examination shows a loosening of 
the muscle cells from one another, as if by some change in the cement 
substance — segmentation — or the fibres may be broken across— fragme^ita- 
tion. The significance of this alteration is not yet fully established, for 
though in some cases it is associated with degeneration and other changes 
in the heart muscle, in others these are not present and the alteration 
may be agonal, or it may in some instances be due to post-mortem 
changes. ^ 

THROMBOSIS AND EMBOLISM OF THE CORONARY ARTERIES. 

Thrombosis. — This may occur in association with endarteritis of the 
coronaries or from their occlusion at their orifices, either by inflammation 
of the aorta or by vegetations or clots on the aortic valves. While the 

^Consult Hektoen, Am. Jour. Med. Sciences, vol. cxiv., p. 555, 1897, bibliography. 
MacCalhim, Jour. Exp. Med., vol. iv.. p. 409, 1899, bibliography. 



THE CIRCULATORY SYSTEM. 403 

blocking of one main trunk of the coronary artery may cause sudden 
death this is not always the case. The interventricular branch of the 
left coronary artery is the most frequent seat of thrombosis, so that in- 
farction which usually follows thrombosis is most often situated in the 
anterior wall of the left ventricle and the lower portion of the interven- 
tricular septum. The characters of such infarctions and the processes 
which follow are given below. 

Embolism of the coronary arteries is much less common than thrombo- 
sis and may be followed by similar lesions of the myocardium. Infec- 
tive emboli are frequent excitants of suppurative lesions of the myocar- 
dium. 

INFLAMMATION. 

Myocarditis. 

The inflammatory changes in the walls of the heart involve primarily 
the interstitial tissue and blood-vessels, the muscle fibres being secon- 
darily affected by atrophic and degenerative changes. 

Interstitial Myocarditis may be acute and suppurative, or chronic with 
the formation of new connective tissue. 

Acute Suppurative Myocarditis may be diffuse, infiltrating the wall of 
the heart with pus. This may occur as a complication of infectious dis- 



FiG. 316.— Bacterial Embolus in Heart Muscle. 

The bacteria have multiplied since lodgment in the small vessel, so that the latter is widely distended. The 

surrounding muscle is necrotic. 

eases, such as scarlatina, diphtheria, typhoid fever, gonorrhoea, ' or may 
be associated with ulcerative endocarditis. * 

More frequently the suppurative inflammation is circumscribed, re- 
sulting in abscesses. These occur with j)y8emia, mycotic ulcerative endo- 
carditis, and other infectious diseases. They are of different sizes and 
either single or multiple. They are produced by the lodgment of infec- 

^For a consideration of gonorrhceal myocarditis, consult Councilman, American 
Journal of the Medical Sciences, vol. cvi., p. 277, 1893. 

'^ For a special study of this mode of origin see Josserand and Bonnet, Arch, de 
Medecine exp. et d. Path, anat., t. xi., p. 570, 



404 THE CIRCULATORY SYSTEM. 

tious emboli in small vessels. There is at first necrosis of the mnscle 
fibres near the bacterial mass (Fig. 216), followed by local suppuration 
and the formation of abscess. The contents of the abscesses consist of 
pus, broken-down muscle tissue, and bacteria.' These abscesses may 
open into the pericardial sac and set up a purulent pericarditis ; or into 
a heart cavity, giving rise to thrombi in the heart and infective emboli in 
different parts of the body ; or the wall of the heart is weakened by the 
abscess so that it ruptures, or an aneurismal sac is formed ; or an abscess 
in the interventricular septum may establish an opening between the 
ventricles ; or the suppurative process may extend upward and form an 
abscess in the connective tissue at the base of the heart. Streptococcus 
and staphylococcus pyogenes are the most common excitants. 

In rare cases the patients recover, the contents of the abscesses be- 
come dry and hard, and enclosed by a wall of fibrous tissue, or the con- 
tents may be absorbed and the whole replaced by fibrous tissue. 

Chronic Interstitial Myocarditis may be associated with chronic peri- 
carditis or endocarditis ; but in a large proportion of cases it occurs in 
connection with lesions of the coronary arteries. 

When through obliterating endarteritis, atheroma, thrombosis, or 
embolus of a branch of the coronary arteries, ^ the blood supply is cut off 
from a circumscribed portion of the heart wall, the tissue in the afi"ected 
area may undergo fatty degeneration, leading to rupture.'' Or, instead 
of extensive fatty degeneration, the cutting off of the blood supply from 
a limited region may result in necrosis — lohite infarction. These areas, 
grayish in color, often slightly projecting from the surface, are fre- 
quently surrounded by a red zone of hypergemia. The nuclei of muscle 
and fibrous tissue fail to stain, the muscle cells become necrotic, lose 
their striation and degenerate, and may be absorbed or gradually replaced 
by fibrous tissue. When larger areas are involved, the muscle fibres 
may break down into a granular detritus and the connective tissue about 
them suffer degeneration or necrosis, so that the whole affected area may 
be soft and yellowish-white or grayish in color. If, as not infrequently 
occurs, there is considerable extravasation of blood, the degenerated 
area may be of a dark red color. ' Under these conditions the heart wall 
may rupture, or acute inflammatory x)rocesses may occur, or the de- 
generated tissue may be gradually absorbed and replaced by granula- 
tion tissue formed from the surrounding fibrous tissue and blood-vessels. 

^ For a detailed consideration of tlie formation of such embolic abscesses, see p. 113. 

^ According to Sternberg, the right coronary artery supplies the following regions 
of the heart • most of the right auricle ; the posterior part and most of the anterior part 
of the right ventricle ; most of tlie interauricular and interventricular septa ; the pos- 
terior part of the left ventricle and the posterior papillary muscles. The remainder of 
the heart is supplied by the left coronary artery. 

While there are superficial anastomoses between the larger trunks of the coronary 
arteries, their branches do not communicate after they enter the heart muscle. 

^ Through the Thebesian vessels sufficient nutriment may reach the myocardium to 
maintain the muscle for a time, even with considerable lesion of the coronary arteries. 
See Pratt, American Journal of Physiology, vol. i., p. 86, 1898. Also Baumgarten, 
ibid., vol. ii., p. 243, 1899. 

^This condition of the heart is often called "myomalacia." 



THE CIRCULATORY SYSTEM. 405 

This gradually grows dense, shrinks, and assumes the characters of cica- 
tricial tissue. 

This may occur in any part of the heart wall or in the papillary mus- 
cles, but is most common in the region supplied by the anterior coronary 
arteries. When the heart wall is involved the new-formed connective 
tissue may yield to the blood pressure from within and aneurism of the 
heart be formed. 

Impaired nutrition of a portion of the heart wall as the result of nar- 
rowing or obliteration of the coronary arteries or their branches, whether 
it lead to such extreme lesions as those just described, or to fatty degen- 
eration, or to atrophy of the muscle cells with a production of new con- 
nective tissue, is of great significance, and it may be the dominant factor 
in many cases of sudden death. 

Occasionally there is a formation of new connective tissue in the 
myocardium as well as in the endocardium without evident lesion of tne 




Fig. 217.— Chronic Interstitial Myocarditis. 

Showing transverse section of a portion of a papillary muscle. The fibrous tissue is dense and the muscle 

fibres are atrophied. 

coronary arteries or the above-mentioned conditions. This growth may 
be in the form of circumscribed patches (Fig. 217), or diffused over a 
considerable part of the wall of the heart ; in both instances with atrophy 
of the muscle. Such an interstitial inflammation is often followed by 
dilatation of the cavities of the heart, by the formation of aneurisms of 
the wall of the heart, and of thrombi in the cavities of the heart. 

It is believed by many observers that the new connective tissue which 
develops in the heart in connection with atrophy of the muscle fibres, as 
a result of imj)aired nutrition due to a narrowing of the lumen of the 
coronary arteries, is not in the stricter sense inflammatory in its nature, 
but is rather a ^&roMS hi/j^erjylasia, the new-formed connective tissue form- 
ing secondarily, to replace the muscle fibres which have atrophied. It 
is interesting in this connection to note that under these conditions the 
muscle fibres immediately beneath the endocardium and close around the 
blood-vessels where the nutritive supply is most abundant are often not 
atroj)hied, nor is the growth of connective tissue marked. 



406 



THE CIECULATOEY SYSTEM. 



Tuberculous Myocarditis is of occasional occurrence and may be asso- 
ciated with tuberculosis of the pericardium or endocardium. ' 

Syphilitic Myocarditis is accompanied by the growth of connective tis- 
sue or granulation tissue in the wall of the heart between the muscle 
fibres. The pericardium and endocardium may also be thickened, and 
pericardial adhesions may be formed. Gummata of the heart are of rare 



occurrence. 



Endocarditis. 



The endocardium is a connective-tissue membrane containing but few 
blood-vessels which lines the cavities of the heart and forms its valves. 
Its inner surface is covered with a layer of endothelial cells. The con- 
nective-tissue cells and basement substance are principally concerned in 
the inflammatory processes. The new tissue thus produced is prone to 

degeneration and calcification. 
The roughening of the endo- 
cardium due to the inflammation 
often leads to the formation of 
fibrin on the affected surface. 

The endocardium which 
forms the valves is that which 
is most frequently involved, but 
the other portions of it are by no 
means exempt. 

In foetal life it is the endo- 
cardium of the right heart, in 
extra -uterine life that of the left 
heart, which is usually affected. 
1. Simple Acute Endocarditis. 
— This is frequent with rheuma- 
tism, but may occur under other 
conditions. It may occur in a 
heart previously healthy, or in 
one already the seat of chronic 
endocarditis. 

In some cases the only lesion 
is a simple swelling of the 
valves. These are thick and 
succulent, but their surfaces remain smooth. The basement substance is 
swollen, and there is a moderate production of new connective-tissue 
cells. In other cases the growth of connective-tissue cells is more marked, 
the basement substance is split up, and little cellular fungous masses of 
connective tissue called ^'vegetations,'' project from the free surface of 

1 Consult Moser, "Tuberculosis of the Heart." Reports of the Boston City Hospi- 
tal, eleventh series, p. 194, 1900. 

^SeeLoomis, Am. Jour. Med. Sciences, vol. ex., p. 389, 1895, bibliography. Also 
Adle)% Trans. Assn. Am. Phys., vol. xiii., p. 73, 1898, bibliography. 




Fig. 218.— Ulcerative Endocarditis. 

The valve and adjacent portion of the heart wall Is ul 
cerated, and a ragged clot has formed upon the rough 
ened surfaces. 



THE CIRCULATORY SYSTEM. 407 

the endocardium. On these roughened surfaces the fibrin of the blood is 
deposited, and thus vegetations of considerable size may be formed (see 
Fig. 218). In still other cases the cell growth, while in some places 
forming vegetations, in other places degenerates, and thus portions of 
the valves are destroyed. This is simple acute ulcerative endocarditis. 

In some cases of this disease the patients recover and the valves seem 
to return to a normal condition ; in other cases the valves are left perma- 
nently damaged ; and in still others chronic endocarditis follows the 
acute form. 

2. Mycotic or Malignant Endocarditis (Malignant Ulcerative Endocardi- 
tis). 

The direct excitants of simple acute endocarditis of the forms described 
above are unknown, but in a considerable number of cases of acute 
endocarditis bacteria have been found in and about the vegetations, and 
proved, by careful experiments, to stand in a causative relation to the 
lesion. 

Those cases of acute endocarditis in which the lesions are induced by 
the direct action of bacteria are called mycotic or malignant endocarditis ; 
or, since the new-formed as well as the old tissue about the bacteria is 
apt to become necrotic and thus lead to larger or smaller losses of sub- 
stance, the lesion is often called malignant ulcerative endocarditis. Cases 
of multiple aneurism in connection with mycotic endocarditis have been 
reported. Various species of bacteria may be excitants of malignant 
endocarditis. 

It is most commonly induced by Staphylococcus pyogenes aureus and 
Streptococcus pyogenes. Micrococcus lanceolatus, B. typhosus, B. tu- 
berculosis, B. anthracis. Micrococcus gonorrhoeae, ' and others have been 
occasionally found. ^ 

It has been, furthermore, found that a lesion or injury of the endo- 
cardium, either on the heart valves or elsewhere, predisposes to the lodg- 
ment and growth upon it of pathogenic bacteria when once they have 
gained access to the circulating blood. ^ 

Mycotic endocarditis is frequently a secondary complicating lesion, 
but may occur as a primary disease. It is most apt to be associated 
with the acute infectious diseases, and may be one of the local manifes- 
tations of pyaemia. 

In some cases there is a formation of new tissue in the form of organ- 
ized vegetations on the valves or general endocardium ; in other cases 
necrosis either of the new-formed or the old tissue is the most marked 
feature. Thrombi are apt to form on the affected surfaces and often 
largely make up the so-called vegetations. The mitral and aortic valves 
are frequently the seat of the lesion, but it may occur elsewhere. 

^ For references and bibliography of gonorrlioeal endocarditis see Lartigau, Am. 
Jour. Med. Sciences, vol. cxxi., p. 52, 1901. 

2 For a general consideration of the pathology of infective endocarditis see Wash- 
5o?<^r?i and others, Brit. Med. Jour., November 4, p. 1269, 1899. 

" For a study of local predisposing factors in malignant endocarditis see Prudden, 
Am. Jour. Med. Sciences, vol. xciii., p. 55, 1887. 



408 



THE CIRCULATORY SYSTEM. 



Detachment of bacteria containing fragments of the vegetations or 
clots may give rise to single or multiple infectious emboli and abscesses 
in various parts of the body, such as the spleen, kidneys, brain, skin, 
heart wall, etc. Bacteria similar to those in the heart lesion may be 
found in these secondary abscesses. 

It is i)robable that abscesses in ulcerative endocarditis do not always 
arise from cai^diac emboli, but may precede the heart lesion. 

3. Chronic Endocarditis may succeed acute endocarditis, or the inflam- 
mation may be chronic from the outset. It affects most frequently the 

aortic and mitral valves, and the endocardium 
of the left auricle and ventricle; similar 
changes in the right side of the heart being 
much less frequent. 

There are two main anatomical varieties 
of chronic endocarditis, which may occur 
separately or together. 

(1) The endocardium is thick and dense, 
its surfaces are smooth or 
covered with small, hard 
vegetations or ridges (Fig. 
219) ; it is often infiltrated 
with the salts of lime. 

(2) There is a growth 
of connective -tissue cells in 
the endocardium, with a 
splitting-up of the base- 
ment substance. Some of 
the new cells continue to 
live, others degenerate. 
By the combination of such a cell growth and 
destruction the endocardium is in some places 
destroyed, in others changed into projecting 
vegetations (see Fig. 220). Fibrin is depos- 
ited on the roughened surfaces (Fig. 221). 
After a time the condition may be further 
complicated by the shrinkage and deposition 
of the salts of lime in the new tissue and in 
the endocardium. All these changes may extend to the wall of the heart 
beneath the endocardium. 

The most important result of chronic endocarditis is its effect on the 
heart valves, producing insufficiency and stenosis. The changes in the 
valves are followed by changes in the walls and cavities of the heart, and 
disturbances of the circulation throughout the body. 

4. Chronic Ulcerative Endocarditis. — Large ulcers or perforations of 
the valves may be formed in chronic endocarditis, upon which clots niaj^ 
form, so that in gross appearance a great similarity exists between this 
and malignant ulcerative endocarditis, particularly if the latter have been 




Fig. 319.— Chronic Endocarditis. 

Showing thickening of the cusp of 
the aortic valve. 



THE CIRCULATORY SYST:eM. 



409 



M 




Fig. 220.— Vegetation on Aortic Valte in Endocarditis. 
Showing granular thrombus over the surface. 



engrafted upon an already chronically diseased endocardium. The 
microscopical and biological examinations must usually be resorted to in 
order to determine the exact significance of the lesion. 

5. Tuberculous Endocarditis may occur in connection with tuberculous 




Fig. 221.— Chronic Endocarditis. 
Showing fibrous "vegetation " on the mitral valve. "With a large blood clot formed upon it. 



410 THE CIRCULATORY SYSTEM. 

pericarditis or general miliary tuberculosis. The tubercles may be small 
and single, or grouped in masses, and show the usual degenerative 
changes. ' 

TUMORS. 

Primary tumors in the heart are rare, but sarcomata, myxomata, fibro- 
mata, and lipomata may occur. Rhabdomyomata, probably congenital, 
may occur in the heart wall as circumscribed nodular masses.^ A cav- 
ernous tumor of this kind has been described. Secondary tumors, as a 
result of metastasis or of continuous growth from the pleura or other 
adjacent parts, are not very infrequent. These are usually carcinomata 
or sarcomata. Secondary chondromata have been observed. ' 

PARASITES. 

Echinococcus sometimes occurs in the heart wall and may perforate 
into the cavities. Cysticercus cellulosse has been observed. 



The Blood-Vessels. 

ATROPHY AND HYPERTROPHY. 

Atrophy of the blood-vessels may involve the entire trunk or some 
of its elements. It may occur as a part of general malnutrition of the 
body, or in connection with atrophy of particular organs, or as an accom- 
paniment of various diseases of the vessels themselves. 

Hypertrophy, which is especially seen in the arteries, may occur in the 
establishment of a collateral circulation upon the closure of arterial 
trunks: or it may occur as the result of increased blood pressure, as in 
some forms of hypertrophy of the heart. 

The Arteries. 

RUPTURE AND WOUNDS. 

The arteries are predisposed to rupture by fatty degeneration, arterio- 
sclerosis with atheroma, and in various forms of acute inflammation. 
Stenosis of the aorta may be followed by rupture between the occlusion 
and the heart. The rupture may be complete or a dissecting aneurism 
may form (see page 419). Eupture of the aorta may lead to sudden 
death. There may be partial or complete rupture of an artery from con- 
tusions, wrenchings, falls, etc. The injury to an artery from a penetrat- 

^ See reference, Moser, p. 406. Also Etienne, Arch, de Med. Exp., vol. x., p. 146, 
1898. 

'^ Seiffert, Ziegler's Beitr., Bd. xxvii., p. 145, 1900, bibliography. 

^For bibliography of heart tumors consult Berthenson, Arch, de Med. Exp., vol. 
v., p. 386. 



THE CIECULATOEY SYSTEM. 411 

ing wound may be fatal if the vessel be large. The wound of a small 
artery may close or a false aneurism may develop at its seat. 

In the healing of a wounded artery the vessel retracts and contracts, 
and a thrombus is formed within it. The contraction may be alone suffi- 
cient to close the vessel ; its coats thicken, and the inner surfaces finally 
are fused together ; or the blood coagulates and forms a thrombus in the 
vessel near the wound. This thrombus later becomes organized and the 
vessel is converted into a fibrous cord. 



DEGENERATION. 

Fatty Degeneration. — This may occur in the walls of otherwise unal- 
tered vessels, or in those which have undergone a variety of inflamma- 
tory or degenerative changes. It may occur either in the intima or 
media, or both, and may be so extensive as to form a very prominent 
gross lesion, or so little developed as to require the microscope for its 
recognition. When marked, especially if occurring in the intima of 
large vessels, smaller and larger spots or stripes or patches may be seen, 
of a yellowish-white color, usually sharply circumscribed, and sometimes 
smooth, sometimes roughened on the surface. It is most apt to occur in 
the aorta, but may be found in any of the vessels. In moderate degrees 
of the lesion we find on section that the cells of the intima contain fat 
droplets in greater or less number. When further advanced, not only 
are the cells crowded with fat droplets, but the intercellular tissue also 
maj' be more or less densely infiltrated with them. Sometimes the infil- 
tration is so dense that the tissue breaks down, and there may be an ero- 
sion of the surface, forming a so-called fatty ulcer. When the media is 
involved the muscle cells contain fat droplets. It may lead to the for- 
mation of aneurism or to rupture of the vessels. 

Amyloid Degeneration, which may affect all the coats of the arteries, 
but especially the intima and media, has already been described in gen- 
eral (page 82). It will be further considered under the lesions of the 
organs in which it most commonly occurs. 

Hyaline Degeneration may cause thickening of the intima of the blood- 
vessels by its conversion into or infiltration with a homogeneous material 
somewhat similar to amyloid (see page 86). Or it may involve the entire 
wall of smaller vessels, converting them into irregular lumpy cords. 
The lumen of vessels thus changed may be obliterated or occluded by 
thrombi. 

Calcification usually occurs in vessels otherwise diseased, and may 
involve either the intima or media. It consists in the deposition of salts 
of lime either in the cells or intercellular substance. The lime may be 
in the form of larger or smaller granules or in dense translucent plates. 



412 



THE CIECULATOKY SYSTEM. 



INFLAMMATION. 






¥iG. 233.— Chronic Arteritis— Arterio- 
sclerosis— Obliterating Endarteritis. 

Showing a thickening of the intima in a 
small artery of the brain. 



Acute Arteritis. — Acute inflammation of the walls of the arteries is, in 
the majority of cases, the result of injury, or of an inflammation in the 

vicinity of the vessel, or of the lodg- 

__' _ ^ nient within it of some foreign body of 

.. ^ , ' .,- ^ an irritating or infectious nature. The 

^^, - ^ ^ inflammatory process may be largely 

" ''','' ^ confined to the inner coat of the ves- 

^ (* ' I sels — endarteritis ; or it may commence 

^ ; ^ ' \ in the outer coats — periarteritis; or it 

may involve the entire wall. 

The blood-vessels in the outer coats 
may be congested, the tissue oedema- 
tous and infiltrated with pus cells, and 
the entire wall may become necrotic. 
The intima, if this layer be involved, 
loses its natural gloss and looks dull 
and is swollen. Under these conditions 
thrombi usually form, and in these may 
occur the various changes which have 
been already described on page 73. 
Chronic Arteritis (Arterio-Sclerosis) , — Since the publication of the 
studies of Gull and Sutton on arterio- capillary fibrosis, attention has been 
every year more and more directed 
to chronic pathological changes in 
the arteries as of great frequency 
and importance. These changes 
are productive and degenerative in 
character and have an important 
bearing upon the circulation and 
upon the integrity of the vessel 
walls. They are in part primary, 
in part secondary, and may involve 
single vessels or vascular territories 
or may affect the entire vascular 
system. 

The lesions differ somewhat in 
the small and large vessels. In 
very small arteries there is a more 
or less general though not uniform 
thickening of the intima (Figs. 222 
and 223). This is due in part to a 

proliferation of the endothelium, in part to increase in the connective 
tissue of the intermediary layer. In this way a considerable amount of 
moderately cellular fibrous tissue (Fig. 224) may form within the mem- 



^'' 



Fig. 



233. — Chronic Arteritis — Arterio-Scle- 
rosis— Obliterating Endarteritis. 



The new-formed tissue is most abundant at one 
side of the vessel, where the external coats are 
pouched. There is degeneration of the new-formed 

tissue. 



THE CIRCULATORY SYSTEM. 



413 



brana elastica, and the lumen may be largely or wholly obliterated — 
obliterating endarteritis. The middle coat as well as the inner may be 
thickened (Fig. 225). 

In larger arteries the new tissue may form beneath the endothelium 
diffusely or in circumscribed masses, or may encircle the vessel. The 
endothelium over the involved areas 
may remain intact or it may prolifer- 
ate or become fatty or necrotic. The 
new-formed fibrous tissue of the in- 
tima, which may contain also new elas- 
tic fibres, ' is usually dense, having few 
cells, and is prone to undergo fatty de- 
generation, to become necrotic, and 
to disintegrate, and thus larger and 

smaller cavities filled with disintegrated tissue, fat, and cholestearin 
crystals, may develop in the new-formed tissue (Figs. 223 and 226). 
These are called atheromatous cysts. ^ They may extend toward the lumen 
of the vessels into which they may open, giving rise to emboli and 




Fig. 224.— Connective Tissue Formed in 

THE INTIMA IN ARTERIO-SCLEROSIS. 




Fig. 225.— Chronic Arteritis. 
Inner and middle coat thickened— radial artery. 



forming rough-edged ulcers, often with undermined edges. Upon these 
thrombi may form. In the new -formed tissue of the intima as well as 



^ See Jores, Ziegler's Beitr., Bd. xxiv., p. 458, 1898, bibliography. 

'^ The word atheroma is sometimes applied to the whole process of arterio-sclerosis, 
but it would be well to limit it to the degenerative phases which result in softening of 
the tissues. 



414 



THE CIRCULATORY SYSTEM. 



in the necrotic foci and in the detritus of the cysts calcification may 
occur. 

Fatty degeneration, atrophy, and calcification may occur in the mus- 
cularis and adventitia of the involved vessels. 

Similar processes may occur in the aorta, the new tissue growth and 




Fig. 236.— Chronic Arteritis— Arterio-Sclerosis— Cerebral Artery. 
Inner coat thickened ; degeneration and softening (atheroma) of a part of the thickened area. 

the degeneration being less definitely limited to the inner layer of the 
wall. The aorta may thus be beset with larger and smaller irregular, 
white, hard, elevated thickenings (Fig. 227), often yellowish from fatty 
degeneration. Beneath these there may be atheromatous softening, or 




Fig. 337.— Chronic Inflammation of the Aorta— Atheroma of the Aorta. 
Showing on the inner surface patches of new-formed tissue— ulceration and calcification. 



THE CIRCULATORY SYSTEM. 415 

these sclerotic areas may be calcified and project as hard, often brownish, 
plates with smooth or rough edges. The surface of the aorta may be rough 



Fig. 228.— Chronic Inflammation of the Aorta— Atheroma of the Aorta. 

Section showing involvement of all the layers. The thickening of the intima is irregular and areas of 
degeneration are seen in its deeper portion. Patches of • flbrous tissue are present in the muscularis. A 
small thrombus is formed upon the surface. 

from erosion over the degenerated areas, and upon these or elsewhere 
parietal thrombi may form (Fig. 228). Such sclerotic areas are often 
well marked at the junction of smaller vessels with the aorta. 

We have seen that in the smaller vessels arterio- sclerosis may lead to 
extreme narrowing or occlusion of the lumen. When this does not occur, 
and especially in the medium -sized arteries, since the new tissue is less 
elastic than normal and liable to yield to the i)ressure of the blood, the 
lumen may in places be dilated (Fig. 229) or the wall may rupture. In 
this way aneurisms may form. This is especially apt to occur when 











> J-^:^^^^ Iri' 



Fig. 229.— Chronic Arteritis— Arterio-Sclerosis. 

Showing pouching of the wall of the artery at the side on which is the largest formation of new flbrous 

tissue. 

atheromatous degeneration has taken place and the muscularis is either 
atrophied or degenerated. In the aorta also dilatation and rupture may 
occur. 

Arterio -sclerosis may be largely limited to the aorta or to other single 
vessels, or it may occur in special vascular tracts, such as those of the 
brain or heart. 



416 THE CIRCULATORY SYSTEM. 



Periarteritis Nodosa. 



A few cases have been described in which many of the small arteries in the muscles 
and in the viscera were beset with small white knobs projecting from the side or sur- 
rounding the vessels. These circumscribed thickenings of the vessel wall are apt to 
involve all the layers of the vessel, and may encroach upon the lumen. The thickened 
portions are infiltrated with small spheroidal cells. Multiple aneurisms may develop 
at the seat of the local thickening. ^ 

The CoNDiTioisrs Leading to Arterio- Sclerosis. — The lesious of 
arterio- sclerosis often occur with gout, syphilis, chrouic lead and alcohol 
poisoning, overwork and overfeeding. They are usual in senility, and 
predisposition to them may be inherited. They may be associated with 
cardiac hypertrophy from valvular lesions or with chronic diffuse ne- 
phritis or other conditions involving increased arterial tension. They 
may occur locally in connection with tumors. 

While the mechanical conditions under which arterio -sclerosis devel- 
ops are not very fully understood, the studies of Thoma have pointed 
the way along which fruitful research may be confidently expected. 

In accordance with the results of Thoma 's experiments one may le- 
gard the primary lesions of arterio-sclerosis as a compensatory hyperpla- 
sia of the intima. For example, if for any reason the wall of the artery 
in a given region, as is the case in the circumscribed or nodular forms of 
arterio-sclerosis, be weakened and yields to the blood pressure, it is at 
this point that the new tissue forms in the intima and restores the lumen 
to its natural calibre (see Figs. 223 and 229) with restitution of the rate 
of blood flow. That this compensation is often incomplete or tempo- 
rary, or that it brings with it other and often serious complications, does 
not militate against this view of the significance of these blood-vessel le- 
sions, and is only one of many examples of imperfect adaptation in path- 
ological processes.^ 

Classification of the Forms of Arterio-Sclerosis. — Various 
classifications of the lesions of arterio-sclerosis have been made. Thoma' 
places in one class the primary and more limited nodular forms of fibrous- 
tissue growth, especially in the larger vessels, which he regards as com- 
pensatory in the way just indicated ; in another the diffuse or secondary 
form, which is attributable to an increased resistance to the flow of blood 
in peripheral vessels, such as those of the kidney, a weakening of the 
muscularis through degeneration, the consequent dilatation, and then 
the compensating fibrous-tissue growth in the vessels at large. 

Councilman* has grouped the lesions into three forms: 1st, the nodu- 

^Consult V. Kahlden, Ziegler's Beitrage z. path. Anat., etc., Bd. xv., p. 581, 1894; 
also Graf, ibid., Bd. xix., p. 181, 1896. 

^ See reference to Welch, p. 127. 

^ Thoma, see Virch. Arch., Bd. xciii., p. 443; ibid., Bd. cxvi., p. 1; also Thoma's 
"Text-Book of General Pathology," vol. i., Eng. trans. 

■^Councilman, Trans. Assn. American Physicians, vol. vi., p. 179, 1891. Council- 
man gives a resume of views based upon Thoma's studies. 



THE CIRCULATORY SYSTEM. 



417 



lar, corresponding with the primary form of Thoma ; 2d, a senile form, in 
which there are often great distortion of the vessels, calcification, and f re- 
qnent thinning of the walls. Atrophic changes in the viscera are apt to 
be associated with this form of senile arteritis; 3d, a diffuse iovm. of 
marked obliterating endarteritis with fibrons involvement of the muscu- 
lar layer. This is apt to be associated with hypertrophy and often with 
dilatation of the heart, and with chronic diffuse nephritis often with atro- 
phy. The arterial changes may be marked in the liver as well as in the 
kidneys. 

Tuberculous Arteritis. — Tuberculosis of the arteries is usually second- 
ary, the process extending to their walls from an already established 




Fig. 230.— Tuberculous Arteritis ix the Lung. 

Showing the encroachment of an area of tuberculous inflammation upon the wall of the artery and the 
formation of a mass partly occluding the lumen of the vessel. This section shows how the generalization of 
the tuberculous inflammation through the body may occur by the sweeping away of the tubercle bacilli by 
the blood and the establishment of new foci in various parts of the body. 



focus (Fig. 230). Tubercle tissue with necrosis may involve the external 
layers, while an obliterating inflammation often closes the lumen. Thus 
it is that in tuberculous cavities of the lungs large arterial trunks may 
be laid bare (see Plate X. ) without a distribution of the bacilli through 
the body and without haemorrhage. Tuberculosis of the aorta is of occa- 
sional occurrence. ' 

Syphilitic Arteritis. — In the more characteristic forms of this lesion 

^ Stroebe, Centralbl. f. Patliologie, Bd. viii., p. 998, 1897, bibliography. Consult 
Blumer, American Jour, of the Med. Sciences, vol. cxvii., p. 19, 1899, bibliography. 

27 



418 



THE CIRCULATORY SYSTEM. 



there may be gummata formed iu the walls or a diffuse formation of new 
cells and new fibrous tissue, especially in the adventitia of the vessels. 
This may extend to the middle and internal layer and lead to narrowing 
or closure of the lumen. Such lesions may be circumscribed or extensive, 
and may result in aneurism or rupture. ' 

ANEURISM. 



An aiieurism is a dilatation of an artery, either cylindrical, fusiform, 
or sacculated, the walls consisting of all or part of the coats of the artery 
variously altered. 

The conditions which commonly lead to aneurisms are arterio- sclero- 
sis, either with or without associated degeneration, or the local weakening 

of the walls of the vessels 
which often leads to com- 
pensatory arterio - sclerosis, 
or the blocking of a vessel 
by embolus. Aneurism may 
develop at the point of ]3ar- 
tial rupture of the walls of 
an artery. Aneurisms may 
follow the local necrotic and 
ulcerative process in the 
walls of the vessels or on the 
heart valves incited by in- 
fectious agents, which as 
emboli or otherwise have 
reached these parts. 

In cylindrical or fusiform 
aneurism there is apt to be 
at first a distention of all 
the walls of the vessel ; but 
this is often irregular, so 
that the sac may bulge more 
in one place than in another 
(Fig. 231). The walls may 
become thin or through 
new-formed tissue they may 
become thickened ; they may 
undergo degeneration or cal- 
cification. Such aneurisms are most frequent in the aorta, but may oc- 
cur in other vessels. 

In the sacculated aneurism there is either a dilatation of the entire 
circumference of an artery over a short portion of its length ; or there 
may be a dilatation of only a small portion of one side of the wall, so 




Fig. 231.— Fusiform aneurism of the arch of the aorta. 



^ For a careful stuclj^ of alterations of the blood-vessels in syphilis 
Ziegler's Beitr. z. path. Anat., Bd. xxvi., p. 202, 1899, bibliography. 



Abramow, 



THE CIRCULATORY SYSTEM. 419 

that the aneurism looks like a swelling attached to one side of the artery. 
The aneurism may commence as a dilatation of all the coats of the vessel ; 
but the middle coat soon atrophies, so that the wall is composed of the 
inner and outer coats ; or the inner coat is destroyed by endarteritis, so 
that the outer coat alone forms the wall of the aneurism ; or the dilata- 
tion may commence at the seat of rupture of one or more coats of the 
vessels. As the aneurism increases in size it may press upon and lead to 
partial destruction of neighboring tissues and viscera, so that portions of 
these tissues and viscera may take the place of the wall of the aneurism. 
The cavity of the aneurism is filled with fluid or clotted blood, or with 
layers of fibrin which adhere closely to its wall. The communication 
between the aneurism and the artery may be small or large. If arterial 
branches are given off from the aneurism they may remain open or be- 
come plugged with fibrin ; or their walls are thickened and their cavities 
narrowed by endarteritis. Death may occur by the pressure and inter- 
ference of the aneurism with the adjoining viscera, or by rupture. 

Dissecting Aneurisms are those in which, owing to a solution of con- 
tinuity of the inner layers of the artery, the blood gets between the media 
and adventitia, and forces its way for a greater or less distance between 
them. Or it may separate the media into two layers. 

Spurious or False Aneurisms are most frequently connected with ves- 
sels of the extremities. When an artery is wounded the blood escapes 
into the surrounding soft parts, and a cavity is formed filled with blood 
and broken-down tissue. 

The wound in the artery may heal and the effused blood be absorbed ; 
or it may become the seat of secondary inflammatory processes. 

Finally a wall of fibrous tissue may be formed, while the wound of 
the artery remains open, so that there is an aneurismal sac through 
which the blood is constantly pouring. This is called a fcdse aneurism. 

Aneurismal Varix : Varicose Aneurism. — If an artery be wounded, and 
at the same time the vein which accompanies it, we have as the result the 
conditions called aneurismal varix and varicose aneurism. In aneurismal 
varix the artery and vein become adherent at the seat of injury, so that 
the arterial blood passes directly into the vein. There is a smooth, 
rounded opening between the two vessels, the vein is dilated into a sac, 
and the veins emptying into it are dilated and tortuous. In varicose 
aneurism the artery and vein do not communicate directly, but a false 
aneurismal sac is formed between the vessels, into which the blood is 
poured before passing into the vein. Varicose aneurism may also be 
formed by the spontaneous rupture of an aneurism into a vein. The 
aneurism presses against the vein, becomes adherent, and finally rup- 
tures into it. This condition has been observed between the aorta and 
pulmonary artery ; the aorta and inferior and superior vena cava ; the 
popliteal artery and vein; the femoral artery and vein; the splenic 
artery and vena azj^gos ; the internal carotid and sinus cavernosus. 

Cirsoid Aneurism is one formed by the dilatation and lengthening of 
large or small arteries or arterial tracts. The walls of the arteries are 



420 THE CIRCULATORY SYSTEM. 

thinned, the vessels are tortnons and in places sacculated. These 
changes are most frequent in small arteries, especially the temporal and 
occipital. They involve the trunk of the vessel and its branches, or 
may extend to the capillaries and small veins. They form larger or 
smaller tumors beneath the skin. 



ANEURISMS OF THE DIFFERENT ARTERIES. 

The aorta may be dilated over its entire length, or there may be diffuse 
or circumscribed dilatations at any portion of its course ; or there may 
be several aneurisms, situated at different points. The ascending por- 
tion of the arch of the aorta may be uniformly dilated in a fusiform 
shape (Fig. 231), or there may be circumscribed dilatations on its an- 
terior wall, or, more rarely, on its posterior wall. The sacculated aneu- 
risms vary in size and may rupture within the pericardium ; or they may 
form a cavity in the upper part of the ventricular septum and commu- 
nicate by openings into the pulmonary artery and left ventricle ; or they 
may dilate downward between the visceral and parietal pericardium, in 
front of the heart, pushing that organ backward. They may perforate 
into the right or left auricle or right ventricle, the superior vena cava, 
or the i)ulmonary artery; or they may reach a large size, press on and 
erode the right side of the sternum and adjoining ribs, project under the 
skin, and even rupture externally. 

The transverse portion of the arch may be dilated in a fusiform shape, 
or there may be sacculated aneurisms at any jDoint in its wall. The sac- 
culated aneurisms usually reach a considerable size. They press on the 
sternum and ribs in front, or on the oesophagus, trachea, and bronchi be- 
behind. The large arteries given off from the arch may be occluded. 
They cause death by pressure on the air passages, the oesophagus, and 
the vena cava ; or may rupture externally or into the oesophagus, trachea, 
bronclii, pulmonary artery, or pleural cavities. 

On the abdominal aorta aneurisms are usually sacculated. If they 
are situated high up they may project into the pleural cavities; if 
lower down, into the abdomen. They may compress and displace the 
viscera, vessels, and nerves, and erode the vertebrae. They may rupture 
behind the peritoneum, into the peritoneal cavity, the pleural cavities, 
the inferior vena cava, the bronchi, the lungs, the duodenum, the colon, 
the pelves of the kidney, or the posterior mediastinum. Eupture of the 
aorta with the development of a long dissecting aneurism parallel to the 
vessel may give rise to a condition simulating a double aorta. ^ 

The coronary arteries may be dilated throughout, or may be the seat 
of small sacculated aneurisms. ^ These may rupture into the pericar- 
dium, or may lead to rupture of the heart wall. 

The pulmonary arteries are rarely the seat of aneurisms. Diffuse and 

^See case reported by G. P. Biggs, Trans. Xew York Path. Soc, 1897-98, p. 109. 
2 Consult Capp, Am. Jour. Med. Sciences, vol. cxviii., p. 312, bibliography; also 
Griffith, Brit. Med. Jour., February 2, 1901, p. 266, bibliography. 



THE CIRCULATORY SYSTEM. 421 

circumscribed dilatations, however, sometimes occur on the main trunk 
and on the two principal branches of the artery. They do not usually 
reach a large size, but may cause death by rupture. General dilatation 
of all the branches of the pulmonary artery is more common. It is 
found in connection with stenosis of the mitral valves and with compres- 
sion or induration of the lung tissue. Small multiple aneurisms — miliary 
aneurisms — may occur in the cerebral arteries; less frequently in the 
pulmonary and mesenteric. These are probably due to some congenital 
weakness of the walls at the point of formation of the aneurism. 

Of the other arteries of the body there is hardly any one which may 
not become the seat of an aneurism. ' 



STENOSIS AND OBLITERATION OF THE AORTA. 

This lesion near the entrance of the ductus arteriosus has been observed 
in a considerable number of cases. The degree of stenosis varies. The 
aorta may be entirely closed and converted into a solid cord for a half an 
inch ; or there may be a constriction through which there is a larger or 
smaller opening. The walls of the aorta at this point may be thickened 
and sclerosed. The ductus arteriosus may be closed or open. Above 
the constriction the aorta is usually dilated ; below it, it is normal, dilated, 
or stenosed. 

Stenosis of the aorta is followed by hypertrophy of the left ventricle, 
and, later, of the right ventricle, with venous congestion throughout the 
body; or there may be a collateral circulation developed between the 
arteries given off above and below the constriction ; or there may be rup- 
ture of the aorta, the right ventricle or auricle. 

This condition is found at all ages, but is induced during foetal life 
or in the first year of extra-uterine life. It is probable that it may be 
caused after birth by an abnormal closure of the ductus arteriosus. This 
vessel normally becomes closed without the formation of a thrombus. 
If a thrombus be formed it may extend into the aorta and obstruct it ; or 
the ductus arteriosus is filled with a thrombus, but increases for a time 
in size ; afterward, as the thrombus is absorbed, the vessel contracts and 
draws the walls of the aorta together. 

TUMORS OF THE ARTERIES. 

Secondary tumors, chiefly carcinomata and sarcomata, may occur in 
the walls of the arteries hj continuous growth from without, involving 
first the external layers. To these layers they are usually confined, for 
the density of the inner layers affords such marked resistance to the in- 
filtration of the tumor cells that arteries are apt to pass intact through the 
tumor, which grows around them. More frequently the arteries become 
secondarily involved in the growth of malignant tumors by the occur- 

^ For details concerning form, distribution, and frequency of aneurisms, see the 
larger works on the practice of medicine or surgery. 



422 THE CIRCULATORY SYSTEM. 

reiice within them of emboli formed by larger and smaller masses of 
tnmor cells. 

These emboli are nsnally of small size, and are apt to get into the cir- 
cnlation by growing through the walls of the veins into their lumina. 
Large emboli from tumors are most apt to occur in the branches of the 
pulmonary artery. The emboli, formed as they are for the most part by 
cells callable of growth and proliferation, are apt soon to form connec- 
tion with the walls of the vessels, and, by the growth into them of blood- 
vessels from the vasa vasorum to find the conditions necessary for their 
development, and they may thus soon involve the entire wall of the ves- 
sel and grow out into adjacent parts. 

The Veins. 

DILATATION. (Phlebectasia.) 

Dilatation of the veins, or phlebectasia, presents itself under a vari- 
ety of forms. 

1. Simple Dilatation. — The vein is uniformly dilated in a cylindri- 
cal or fusiform shape ; its length is not increased ; its w^alls may be thicker 
than normal or thinned ; the valves may be thickened, or are insufficient, 
or atrophic, or are torn. 

2. Cirsoid Dilatation. — The vein is cylindrically dilated, but is 
also increased in length, so that it assumes a very tortuous course. The 
walls may be thickened or thinned. 

3. Varicose Dilatation. — Portions of the wall of the vein undergo 
saccular dilatation. The wall of the sac is formed of the coats of the 
vein, but these may be thickened or thinned ; the middle coat may dis- 
ai^i^ear entirely. There may be only one such dilatation, or there may 
be a number on the same vein, or a number of veins may be affected at 
the same time. The vein may be otherwise normal, or, more frequently, 
is more or less uniformly dilated. 

4. Anastomosing Dilatation. — A number of contiguous and 
anastomosing veins are dilated, both, in the cirsoid and varicose forms. 
The vein then looks like a series of cavities sei^arated by thin partitions. 
The dilatations of the same vein become adherent to each other and to 
those of the adjoining veins; portions of the walls of the dilated parts 
may atrophy so that there may be a number of cavities containing venous 
blood and separated from each other by thin partitions. 

Distribution, Causes, and Effects of Phlebectasia. — Sponta- 
neous restitution of dilatations of the veins is not common, and usually 
occurs only in the lesser degrees of the lesion. The tendency of the dila- 
tation is to increase. Thrombi frequently form in the dilated veins, and 
either partially or completely fill them. These thrombi may become 
organized, or they may dry and become calcified, forming j^hleboUths, and 
by the formation of new connective tissue in the walls they may become 
enclosed in a fibrous capsule, with the obliteration of the vessel. The 



THE CIRCULATORY SYSTEM. 423 

wall of the dilated sac may become so thin that it finally ruptures. 
Inflammation of the dilated vein may occur, followed by fibrous thick- 
ening. 

^VTien occurring in mucous membrane, dilated veins are usually asso- 
ciated with persistent catarrh. There is hardly one of all the veins of 
the body which may not be dilated. The hsemorrhoidal veins forming 
^'hgemorrhoids'^; the veins of the leg and thigh; those of the jDclvis and 
pelvic viscera ; those of the sj)ermatic cord, scrotum, and labia ; those of 
the abdominal wall ; those of the neck and arms — are most frequently 
involved. 

The immediate cause of dilatation is usually some obstruction to the 
passage of the blood through the veins toward the heart ; but alterations 
in the walls of the vessels from degeneration, inflammation, or injury 
are often important predisposing factors. 

WOUNDS— RUPTURE. 

Wounds of the veins usually heal by a simple contraction and an 
adhesive inflammation of their walls ; sometimes by the formation of a 
thrombus. Rupture of the veins may be produced by se^^ere contusions 
and crushings of the body and by violent falls. Perforation of a vein 
may be j)roduced by suppuration of the soft parts and the invasion of 
the walls of the vessel ; by the pressure of an aneurism or of a new 
growth ; by the thinning of the wall of the vein in phlebectasia. 

THROMBOSIS. 

Thrombosis of the inferior vena cava has been many times recorded. 
It is usually due to pressure on the vessel or may occur as an extension 
of thrombi from the contributory veins. 

Thrombosis of the superior verui cava usually follows pressure from 
without by tumors, aneurisms, or enlarged lymph nodes. 

Thrombosis of other large venous trunks may occur under various local 
and general conditions (see below, thrombosis and phlebitis, and page 
72).^ 

DEGENERATION. 

Fatty degeneration and calcification may occur in the walls of the veins 
under conditions similar to those in which these changes take place in 
the arteries. 

INFLAMMATION. (Phlebitis.) 

Inflammation of the veins, plileUtis, may involve chiefly the external 
lajyers—2)eri2)Mebitis ; or the internal — endojMebitis ; or, as is very fre- 
quently the case, the entire wall may be affected. Phlebitis may be due 

' For a consideration of peripheral venous thrombosis iu heart disease consult 
Welch, Trans. Assn. Am. Phys., vol. xv., p. 441, 1900, bibliography. 



424 



THE CIRCULATORY SYSTEM. 



to an infectious thrombus, to injuries, or to an infectious inflammation 
of the surrounding tissues. Thrombosis of the vein, either primary or 
secondary, is a very constant accompaniment of phlebitis. Thrombosis 
and phlebitis are not infrequent in association with or following infec- 
tious diseases, in cachectic conditions, and with rheumatism and gout. 

Acute Infective Phlebitis may follow a supi^urative periphlebitis. The 
outer layers of the vein wall are congested, swollen, infiltrated with serum 
and pus. The inner coats may become infiltrated with pus ; they may 
become necrotic and disintegrate. A thrombus is constantly formed under 
these conditions, which may for a time stop the circulation and keep 
the products of inflammation and degeneration and infectious material 
from mixing with the blood ; but the thrombus itself is prone to disinte- 




Fig. 233.— Tuberculous Phlebitis. 
The section Is from one of the pulmonary veins In a child dead of acute general miliary tuberculosis. 



gration, and thus the exudates and fragments of disintegrated thrombi or 
tissue or bacteria may enter the circulation. 

On the other hand, owing to the presence of irritating or infectious 
material within the vein and the formation of a thrombus, the inflamma- 
tory process may be at the commencement an endophlebitis, but usually, 
if the inflammation be at all severe, the entire wall of the vessel is event- 
ually involved. 

Acute phlebitis may terminate in the absorption of the thrombus and 
the return of the vein to its normal condition, or in the obliteration of 
the vein. The pyogenic cocci, the typhoid bacillus, the pneumococcus, 
and several other micro-organisms have been found in phlebitis. In the 
phlebitis with thrombosis, which frequently complicates infectious dis- 
eases such as typhoid fever, pneumonia, etc., the bacteria present are 
frequently not those which are the excitants of the primary disease. 

The most important results of phlebitis are usually those which 
depend upon the introduction into the blood of infectious or other emboli 
(see page 75). The relationship between non-infectious thrombi and 
phlebitis is in many cases not clear. ' 

^Consult in this connection Welch on Thrombosis, Allbutt's "System of Medicine," 
vol. vi., p. 170. 



THE CIRCULATORY SYSTEM. 425 

Chronic Periphlebitis results in thickeniug, principally of the outer 
coats of the veins, but the inner coats may also be involved. The sur- 
rounding tissue may be also thickened and coalesce with the walls of the 
vein. There may or may not be thrombosis. 

Chronic Endophlebitis is a not very common lesion, of the same general 
character as chronic endarteritis, with which it is often associated. 
More or less circumscribed patches of new connective tissue are formed 
in the inner coats, which may undergo fatty or calcareous degeneration. 

Tuberculous Inflammation of the walls of the veins may occur as an 
extension of the process from without or from a lodgment of the tubercle 
bacilli in the blood current on the intima (Fig. 232). This is not infre- 
quent in the pulmonary veins, and Weigert has called attention to the 
fact that in acute miliary tuberculosis the growth of tubercle tissue into 
the lumina of these veins from tuberculous lymph-nodes is of frequent 
occurrence and readily explains the topography and mode of occurrence 
of the general disease. The tubercle bacilli which are present in the 
tuberculous tissue growing into the lumen of the veins find thus an easy 
distribution. ' 

Syphilitic Inflammation may involve the walls of the veins either as 
gummy tumors or as more diffuse thickenings. 

TUMORS. 

Primary tumors of the veins are rare. Small leiomyomata have been 
described in the saphenous and ulnar veins. A myo-sarcoma as large as 
a man's fist has been described, situated in the dilated vena cava inferior. 
The veins are not infrequently secondarily involved by sarcomata and 
carcinomata, and sometimes by chondromata. The thin walls of the veins 
offer comparatively little resistance to the encroachment of malignant 
tumors, which thus gain access to the circulation and may form metas- 
tases in various parts of the body. 

PARASITES. 

Echinococcus is sometimes found in the veins, having either devel- 
oped there or perforated from without. 

Two species of distoma (liver fluke) occur in man. D. hepaticum 
occurs rarely and, while usually found in the bile ducts, may occur in 
the vena cava. D. hcematobium is very common in man in Egypt and in 
other parts of Africa, and usually occurs in the portal vein or its branches, 
and frequently in other veins. 



The Capillaries. 

The walls of the capillaries are so thin and so intimately connected 
with the surrounding tissues that their lesions are studied most appro- 

' See references under Miliary Tuberculosis, p. 218. 



426 THE CIRCULATORY SYSTEM. 

priately among the diseases of the several organs. Dilatation of the 
new-formed capillaries in tumors, granulation tissue, etc., and fatty and 
hyaline degeneration of their walls, may be mentioned here as readily 
observed lesions occurring under a variety of conditions. The changes 
which we assume to occur in the walls of the smaller veins and capillaries 
in exudative inflammation, by reason of which fluids and blood cells pass 
through them, are not yet sufficiently understood to be described with 
definiteness. 

The Lymph- Vessels. 

General Characters of the Lymph-Vessels. 

The smaller lymph-vessels can hadly be treated as independeut structures, since 
their walls are so closely joined with the tissues through which thej pass. It is per- 
haps wiser to follow the suggestion of Adler and Meltzer^ and call the spaces of the con- 
nective and other tissues into which transudation from the smaller blood-vessels takes 
place, not lymph radicles or "lymph capillaries" as is commonly done, but to consider 
them tissue spaces from which the transudates of varying composition are gathered 
into the lymph- vessels. But the larger lymph-vessels we find the seat of various more 
or less independent lesions. 

LYMPHANGIECTASIS. 

Dilatation of the lymph -vessels occurs under a variety of conditions. 
It may be congenital, or it may be due to some hindrance to the flow of 
lymph onward — as by pressure from any cause, or from the occlusion of 
the vessels by inflammation. If the dilated vessels form a circumscribed 
mass, this is often called a lymphangioma (Fig. 170). In certain forms 
of elephantiasis and in macroglossia the dilatation of the lymph-vessels is 
an important factor. Its occurrence is not infrequent in the labia, pre- 
puce, and scrotum. 

Dilatation of the chyle vessels of the mucous membrane of the intes- 
tine and mesentery is of occasional occurrence. 

Obstruction of the Thoracic Duct may be due to tumors, ^ or enlarged 
lymph-nodes, or inflammatory processes in the mediastinum ; to aneurism, 
to thrombosis of the left innominate vein, to insufliciency of the tricus- 
pid valve ; or to inflammatory processes in the wall of the duct. It may 
occur under various other conditions. 

It may be compensated by collateral lymphatic anastomoses, or it may 
lead to various lymphangiectasise and to transudation of lymph. Thus 
chylous ascites may occur. 



INFLAMMATION. (Lymphangitis. ) 

Acute Infective Lymphangitis. — Inflammation of the larger lymph-ves- 
sels is usually secondary and often connected with an infected wound or 

^ Adler and Meltzer, Jour. Exp. Med., vol. i., p. 482, 1896. 

2 For bibliography of carcinoma involving the thoracic duct see A. H. SmWi, Med. 
Record, December 2, 1899, p. 813. 



THE CIRCULATORY SYSTEM. 427 

injury. Owing to the entrance into the lymph trunk of bacteria or other 
infectious agents, poison of venomous reptiles, insects, etc. , the vessels, 
sometimes for a considerable distance away from the wound, become red, 
tender, and painful. Under these conditions the ai:)pearances which the 
vessels present vary. In some cases the redness disappears after death 
and we find no appreciable alteration. In other cases, the walls of 
the lymph- vessels are more or less densely infiltrated with pus cells, 
there is proliferation of the endothelium, and the lumen may contain 
variable quantities of pus and fibrin and desquamated degenerated en- 
dothelium. The tissue about the vessels may also be infiltrated with 
serum and pus. These lesions may undergo resolution and the vessel be 
restored to its normal condition ; or the vessel wall and surrounding 
tissue may die or become involved in abscess ; or new connective tissue 
may form in and about the vessel, sometimes with obliteration of its 
lumen. The associated lymph nodes may participate in the inflammatory 
process. 

Tuberculous Lymphangitis. — Tuberculous inflammation occurs both in 
large and small lymph- vessels. Miliary tubercles and diffuse tubercle 
tissue may form in the walls and project into the lumen of the larger 
trunks ; or in the smaller vessels the new growth may entirely fill the 
lumen, and grow within it, with more or less involvement of the walls. 
This may occur independently, but it is most frequently seen in connec- 
tion with tuberculous inflammation of adjacent tissues. Thus from tuber- 
culous lymph-nodes in the vicinity of the thoracic duct there may be a 
direct extension of the tuberculous inflammation, an involvement of the 
walls of the duct, and a groTvi:h of tubercle tissue into its lumen. Such 
growths in the thoracic duct have been shown by Weigert to occur in acute 
general miliary tuberculosis, and satisfactorily explain the dissemination 
of the tubercle bacilli. In the vicinity of tuberculous ulcers in the in- 
testines, furthermore, we often see the subserous lymph-vessels, which 
pass from the vicinity of the ulcers, distended with the products of tu- 
berculous inflammation and looking like dense white knobbed cords 
(Fig. 291). 

Syphilitic Lymphangitis not infrequently occurs in the vicinity of 
syphilitic ulcers in the primary stage. In later stages there may be 
thickening of the walls of the vessels and the development of gummy 
tumors in and about them. 

TUMORS. 

The relation of the endothelium of the lymph-vessels and spaces to 
endotheliomata has been already mentioned in the section on Tumors. 

The dissemination of malignant tumors through the lymph channels 
is of frequent occurrence, and is particularly marked in the case of car- 
cinoma. In the vicinity of carcinomata the lymph- vessels are not infre- 
quently crowded with the tumor cells, forming white, irregular cords ; 
or small masses of the tumor cells may be found in the lym]3h- vessels. 



428 THE CIRCULATORY SYSTEM. 

either near to or remote from the tumor. White, irregular networks are 
often formed in this way beneath the pleura in carcinoma of the lung 
(Fig. 178), or beneath the capsule of the liver. Transverse sections of 
lymph-vessels thus distended show sometimes swelling and detachment 
of the endothelium and a crowding of the lumen with tumor cells. 



CHAPTER VI. 

THE RESPIRATORY SYSTEM. 

The Nose and its Associated Cavities. 

The mucous membrane lining the nose under normal conditions cleanses from dust 
the air which impinges upon and sweeps across it in respiration. It is in this way ex- 
posed to various deleterious agencies. It is subject also to such sudden changes of 
temperature as may involve great and abrupt alterations in the condition of its blood- 
vessels. 

INFLAMMATION. (Rhinitis.) 

Acute Catarrhal Inflammation is common and often associated with a 
similar process in the pharynx and larynx. There is at first a hypersemic 
swelling followed by an increased prodnction of mncns and transndation 
of sernm from the blood-vessels ; emigration of leucocytes and desquama- 
tion of epithelium may follow. This and other inflammatory processes 
may extend to the frontal sinuses and the antrum where the exudates may 
collect. ' As the process resolves, the exudation ceases, the epithelium 
regenerates, and the mucosa is restored to its normal condition. 

Croupous Inflammation, either sim]3le or diphtheritic, may involve the 
nasal cavities. Phlegmonous inflammation involving adjacent parts is of 
occasional occurrence. Bacteria apparently play an important part as 
excitants of acute catarrhal inflammation. 

Chronic Catarrhal Inflammation may follow the acute form, and is 
marked by hyperi)lasia of the fibrous tissue in the submucosa, often fol- 
lowed by atrophy of the mucosa. Ulceration of the mucosa may occur ; 
the exudate may assume a fetid character ; or, as is frequently the case, 
an hyiDcrplasia of the mucosa, often with a serous infiltration, may lead 
to the formation of the so-called mucous polyps.^ 

Tuberculous and Syphilitic Inflammation with the usual morphological 
characters of these processes are common in the nasal cavities. 

TUMORS. 

Aside from the nasal polyps which may be adenomatous in character, 
the most common tumors are epithelioma and sarcoma. 
Dermoid cysts have been described. 

^ For a study of the bacteriology of nasal inflammation see Howard, Am. Jour. 
Med. Sciences, vol. ex v., p. 520, 1898. 

- For a summary of facts concerning the nature of the ordinary nasal polyps see 
Wright, :N'ew York Med. Record, January 26, 1901, p. 132, bibliography. 



430 THE RESPIRATORY SYSTEM. 

The pharynx may be the seat of lesions similar to those above 
described as involving the nasal cavities (see page 429). 



The Larynx and Trachea. 

Malformations. 

The larynx and trachea may be absent. The larynx may be abnormally large or 
small ; the epiglottis also may be too large or too small, or may be cleft. There may 
be communications between the trachea and the oesophagus, and then the pharynx gen- 
erally ends in a cul-de-sac, and the oesophagus opens into the trachea. There may be 
imperfect closure of the original branchial arches, so that there are fissures in the skin 
leading into fistulee which open into the pharynx or trachea. The fissure in the skin is 
small and is situated about an inch above the sterno-clavicular articulation, usually on 
one or both sides, more rarely in the middle line. Individual cartilages, as the epiglot- 
tis, or one or more rings of the trachea, may be absent, or there may be supernumerary 
rings. The trachea may divide into three main bronchi instead of two, and in that case 
two bronchi are given off to the right lung and one to the left. The trachea may be 
on the left side of the oesophagus or behind it. 



(EDEMA OF THE GLOTTIS. 

This is a condition in which there is an accumulation of serous fluid 
in the submucosa of the upper part of the larynx. This may be due to 
simiDle circulatory disturbances, local or genei^al, or it may be inflamma- 
tory in character. The greatest accumulation of fluid is in places in 
which the submucous tissue is abundant and loose in texture, as in the 
posterior wall of the epiglottis, in the ary-epiglottidean folds, and in the 
false vocal cords. The swelling of these parts may be so great as to 
occlude the air passage. After death the cedematous swelling may 
largely disappear, but the mucous membrane may be left unusually 
wrinkled and flabby. 

Qildema of the glottis is comparatively infrequent in association with 
such heart, kidney, and lung lesions as lead to general oedema. It is, on 
the contrary, frequent in connection with various forms of laryngeal 
inflammation. 

INFLAMMATION. (Laryngitis.) 

Acute Catarrhal Laryngitis. — This occurs as an independent process as 
a complication of the infectious diseases, or may be induced by the inha- 
lation of irritating vapors and of hot steam and smoke. The inflamma- 
tion varies in its intensity in different cases. The mucous membrane is 
at first congested, swollen, and dry; then the mucous glands become 
more active and an increased quantity of mucus is formed. There is 
desquamation of the suiDerficial epithelial cells, while through emigra- 
tion leucocytes may infiltrate the submucosa, and together with mucus 
and desquamated epithelium form the exudate. There may be oedema 
of the glottis. 



THE RESPIRATORY SYSTEM. 431 

After death the congestion of the mucous membrane frequently dis- 
appears altogether. 

Chronic Catarrhal Laryngitis. — The surface of the mucous membrane is 
dry or coated with muco-pus. The epithelium is thickened in some 
places, thinned in others, or in places entirely destroyed. The submu- 
cosa may be infiltrated with cells, diffusely thickened, or form little 
papillary outgrowths; it may be thinned, or necrotic and ulcerated. 

The mucous glands may be swollen and prominent. The inflamma- 
tion may extend to the perichondrium of the cartilages, which may 
become necrotic. In chronic laryngitis there may be a more or less 
diffuse thickening of the epithelium, often associated with an hyperpla- 
sia of the submucous tissue. This is called xxwliydermia diffusa. A sim- 



■^v 



Fig. 233,— Localized Hyperplasia of the Epithelium and Submucous connective Tissue of the 

False Vocal Cords. 

The section shows a portion of a small rough wart-like or papillary growth. 

ilar process, if localized, may lead to larger and smaller wart-like 
excrescences — imchydermia verrucosa (Fig. 233). 

Croupous Laryngitis occurs most frequently as the characteristic local 
lesion in diphtheria, of which the Bacillus diphtheri^e is the excitant (see 
page 235). It may, however, be incited by the Streptococcus pyogenes 
and other bacteria, and not infrequently accompanies other infectious dis- 
eases, scarlatina, typhoid fever, and other exanthemata (see page 186). 
The false membrane may be continuous with a similar structure in the 
pharynx, and it may extend down into the bronchi. 

Phlegmonous Laryngitis. — Su]3purative inflammation involving the 
mncosaandsubmucosaisusually secondary to catarrhal, croupous, tuber- 
culous, or syphilitic laryngitis ; or it may be associated with pyaemia or 
erysii3elas, or it may follow mechanical injury from a foreign body. It 
is not uncommon on the posterior surface of the ei^igiottis or in the ary- 
epiglottidean folds, and may be associated with oedema of the glottis. 
Abscesses may form which rupture into the larynx, or they may extend 
into the neck or the pharynx or oesophagus. 

Tuberculous Laryngitis, — This lesion is most frequently associated with 
pulmonary tuberculosis. Early in the process there is a formation in the 



432 THE RESPIRATORY SYSTEM. 

submucosa of miliary tubercles together with more or less new small - 
celled tissue ; with this is a catarrhal inflammation with an exudate of 
mucus, pus cells, and desquamated epithelium. 

As coagulation necrosis of the subepithelial tubercles occurs, ulcers 
are formed, often with an increase of the catarrhal exudate. The proc- 
ess may extend so as to involve the walls of the larynx, and necrosis of 
the cartilages may follow. Adjacent ulcers may become confluent so 
that considerable areas of the mucous membrane may be destroyed. 

Syphilitic Laryngitis. — This form of inflammation may have the ordi- 
nary characters of an acute or chronic catarrhal inflammation, or it is pro- 
ductive in character with the formation of new tissue in the stroma of 
the mucous membrane. This new tissue is principally composed of 
small cells, which often degenerate and become necrotic. In this way 
the mucous membrane of the larynx and the tissues beneath are thick- 
ened in some places and destroyed in others, giving rise to erosions and 
ulcers. These changes are especially marked in the upper portion of the 
larynx. If the perichondrium be involved there may be necrosis of the 
laryngeal cartilages. Owing to the cicatricial contractions of healed 
syphilitic ulcers there may be great deformity of the larynx. 

Lesions of the trachea are often associated with those of the larynx and 
are in general similar in character. 



TUMORS OF THE LARYNX AND TRACHEA. 

Retention Cysts of the mucous glands of the larynx may form sacs 
projecting into its cavity. 

Papilloma, single or multiple, is the most common form of benign 
tumor of the larynx. It is most frequent upon the vocal cords and is 
usually associated with chronic inflammation. Fibroma, lipoma, myxoma, 
and angioma are occasionally met with. Chrondromata grow from the 
normal cartilages and are usually multiple and sessile. They may pro- 
ject into the cavity of the larynx. 

Fusiform or spheroidal -celled sarcomata of the larynx have been seen 
in a considerable number of cases, both in children and in adults. 

Carcinomata, usually the epitheliomatous type, may originate in the 
larynx, most commonly upon the false vocal cords. But from adjacent 
structures, usually from the oesophagus, cancer may invade the larynx. 

In the trachea tumors are of rare occurrence, but occasional examples 
of growths similar to those in the larynx have been found. Tuberculous 
and otherwise altered bronchial lymph-nodes may by ulcerative processes 
enter and obstruct the trachea. 

Single or multiple amyloid masses, often associated with cartilage, 
have been described in the larynx and trachea. ' 

1 See Manasse, Vircli. Arch., Bd. clix., p. 117, 1900. 



THE EESPIEATOEY SYSTEM. 433 

The Pleura. 

HYDROTHORAX. 

Xon-inflammatory accumulations of clear serum in the pleural cavi- 
ties are of frequent occurrence. They occur under conditions similar 
to those which lead to dropsy in other parts of the body — lesions of the 
heart, liver, and kidneys, and changes in the circulation and in the com- 
position of the blood. 

If the amount of serum be large it may compress the lower lobes of 
the lungs. 

HYDRO-PNEUMOTHORAX— PYO-PNEUMOTHORAX. 

The x^i^esence of air in the pleural cavities is usually associated with 
a serous or i)urulent exudate. It may occur as the result of perforation 
of the lung, from rupture, from ulceration of tuberculous lesions at the 
pleural surfaces, from injuries to the chest wall, perforation of the dia- 
phragm, by suppurative or cancerous lesions of the oesophagus, stomach, 
or intestine, as well as in a variety of other conditions. Gas may form 
in the pleural cavities in infection by the bacillus aerogenes capsulatus. 

H-ffiMORRHAGE. 

Subpleural ecchymoses may occur in asphyxia or during infectious 
diseases or intoxications. More extensive extravasations of blood — 
hiematothorax — may be the result of injuries to the wall of the thorax or 
the rupture of aneurism. 

Hsemorrhagic Exudates are usually associated with tuberculous inflam- 
mation of the pleura or with infarctions of the lungs, carcinoma, or inju- 
ries, infectious diseases, or cirrhosis of the liver. 

INFLAMMATION. (Pleuritis, Pleurisy.) * 

Inflammation of the i)leura may occur as an independent lesion, but 
it is commonly associated with pathological processes in the lungs, peri- 
cardium, abdomen, or chest wall. It may be exudative in character, 
usually associated with more or less proliferation of the mesothelial 
('' endothelial") and connective -tissue cells, or it may be productive 
with the formation of new connective tissue. These phases of inflamma- 
tion may be associated. Through the production of new connective tis- 
sue, repair of the acute inflammatory lesion is commonly effected. In 
the exudative forms of pleurisy the exudate may consist of fibrin, or of 
serum and fibrin, or of serum with fibrin and x)us. 

Simple Fibrinous Pleurisy (Dry Pleurisy ; Pleuritis Sicca). — This may 
involve circumscribed areas of the costal, mediastinal, diaphragmatic, 
or pulmonarv pleura, less frequentlv the entire pleura of one side of the 
28 " 



434 THE EESPIEATORY SYSTEM. 

chest. The affected portions of pleura are dull and lustreless and coated 
with fibrin, opposing surfaces often being joined by bands of fibrin. 
There are swelling, degeneration, proliferation, and exfoliation of the 
mesothelium, with swelling and proliferation of the connective -tissue 
cells beneath. Exceptionally, there is involvement of the entire pleura 
of one side, with the production of such a large amount of fibrin as 
seriously to compress the lung. ' 

Sero-Fibrinous Pleurisy (Pleurisy with Effusion). — This is the most com- 
mon form of pleurisy. As a rule, it involves the greater part of the 
pleura of one side of the chest. Sometimes, however, the pleura of both 
sides of the chest is involved, and then the pericardium also is often 
inflamed. 

While the inflammation is in progress the surface of the affected pleura 
is coated with fibrin, and bands of fibrin stretch between the iDarietal and 
pulmonary pleura. In the pleural cavity is serum in variable quantity. 
This serum is clear, or turbid from the presence of exfoliated mesothe- 
lium, leucocytes, and flocculi of fibrin or red blood cells. The lung is 
comiDressed in different degrees and positions, according to the quantity 
of the serum and the character of the adhesions. The heart may also be 
displaced by the accumulated exudate. 

The natural termination of such a pleurisy is the recovery of the 
patient, with thickenings of the pleura and adhesions. The irregular 
terminations are : The death of the patient, the protracted existence of 
the fibrin and serum, and the change of the character of the inflamma- 
tion so that pus is produced. 

If the patient recover, the serum is absorbed, the fibrin disappears, 
and repair is effected, as in simple fibrinous pleurisy, by the formation 
of granulation tissue, which gradually becomes dense and cicatricial in 
character and may remain as local or general thickenings or firm adhe- 
sions of the opposed pleural surfaces. The lung may be distorted by 
contraction of the new-formed connective tissue. The exudates in the 
sero -fibrinous form of pleurisy do not usually infiltrate the pleura, but 
gather upon its surface and in the cavity. 

The Excitants of Sero -fibrinous Pleurisy. — Cultivations from 
the exudate give in the larger proportion of cases negative results ; but 
the pneumococcus, Streptococcus pyogenes. Staphylococcus aureus and 
albus, and the tyi^hoid bacillus have been isolated. When the inflam- 
mation of the pleura is consecutive to acute lobar pneumonia, the 
pneumococcus may still not be found in the exudate. The presence 
of the streptococcus is frequently followed by the formation of pus. 
The organisms named above may be present alone or in various associa- 
tions. Many cases with simple sero-fibrinous exudate prove on inocula- 
tion to be tuberculous. ^ 

' For a study of the origin of fibrin and adhesions of the serous membranes consult 
Heinz, Virch. Arch., Bd. clx., p. 365, 1900; also Gaylord, Jour. Exp. Med., vol. ill., p. 
1, bibliography. 

2 YoY a study of the bacteria in exudative pleuritis, with the earlier bibliography, 



THE RESPIEATOEY SYSTEM. 435 

Suppurative Pleurisy (Empyema). — Suppurative pleurisy may occur 
either with or without the formation of a considerable sero -fibrinous exu- 
date. The exudate may be purulent from the beginning, or a sero -fibrin- 
ous exudate may assume this character. 

The pleural cavity in empyema is partly or completely filled with 
purulent fluid, and the lung is either compressed against the vertebral 
column or partly adherent to the chest wall. Sometimes, however, the 
purulent fluid is shut in by adhesions, either between parts of the lung 
and the thoracic wall, or between the lung and the diaphragm, or between 
the lung and the pericardium, or between the lobes of the lung. 

The fluid in the pleural cavity is usually a thin, purulent serum, 
composed of serum, i3us cells, mesothelial cells, and flocculi of fibrin ; 
but sometimes this fluid is thick and viscid. 

^Tiile in children the more or less active suppurative x)rocess in the 
pleura may continue for a long time without deep involvement of the 
pleura, in adults granulation tissue may form upon the pleura, which 
thus becomes gradually thickened and may so remain for months with 
its inner vascular surface covered with pus and fibrin. In such cases as 
well as in less chronic forms the fibrin fibrils are often swollen and coa- 
lesce to form irregular homogeneous or finely granular masses. Eesolu- 
tion may occur in one region of the pleura while the exudate in another 
may become encai)sulated by new-formed connective tissue. 

In old cases the thickening of the pleura may be great and it may 
become calcified.' The perichondrium of the cartilages and the peri- 
osteum of the ribs may become inflamed, with necrosis of the cartilages 
and ribs or a production of new bone. Xecrosis and gangrene of the 
involved pleura may occur and putrefactive process be set up in the exu- 
date. The suppurative process may extend from the pleura involving 
adjacent parts, such as the fascise, the muscles, the skin, the diaphragm, 
or the lungs. Thus the pus may find an exit, through the wall of the 
thorax, into the peritoneal cavity or into the lungs. 

In inflammation of the pleura the process may extend to the lymphat- 
ics in the interlobular septa, around the bronchi, and around the blood- 
vessels. This interlobular lymi)hangitis occurs more frequently in chil- 
dren than in adults. The lymphatics in the interlobular septa and those 
around the bronchi and blood-vessels are distended with pus cells, the 
septa are much thickened, and the lobules separated from each other. 

Sero -fibrinous pleurisy and empyema may occur as complications of 
infectious diseases, such as scarlatina, typhoid fever, and various forms 
of septicaemia, or by an extension of an inflammatory process from such 
adjacent parts as the pericardium, lungs, mediastinum, etc. The vari- 
ous forms of pneumonia are frequently associated with local or general 
inflammation of the pleura. 

consult Pnidden, Xew York Medical Journal June 24th, 1893. For fuller data see 
jS'etfe)-, Bouchard and Brissaud's "Traite de Medecine," t. vii., p. 399, 1901. 

'For a resume of our knowledge of various calcifications in the lungs, and allied 
conditions often called "lung stones," consult Polaillon, "Les Pierresdu Poumon," etc., 
Paris, 1891; or Legry, Arch. gen. de Med., March and April, pp. 337 and 466, 1892. 



436 THE RESPIRATORY SYSTEM. 

The Excitants of Empyema. — Streptococcus pyogenes is the most 
frequent excitant of suppurative inflammation of the pleura. Ac- 
cording to the statistics of better this organism has been found in a 
little over forty per cent of the cases examined of all ages. The pneu- 
mococcus has been found in over twenty-five per cent of cases examined. 
The streptococcus and the pneumococcus are associated in a small pro- 
portion of cases. Of less frequent occurrence are Staphylococcus pyo- 
genes, Bacillus typhosus,' Bacillus coli communis, the gonococcus, the 
pneumo -bacillus of Friedlander, and the influenza bacillus. In empy- 
ema with fetid exudate, various forms of bacteria may be present. 
While in the adult the streptococcus is most often found in the empye- 
mic exudate, in young children the pneumococcus is, according to K^et- 
ter,^ most common. 

Chronic Pleurisy with Adhesions. — This form of pleurisy may follow 
one of the varieties of pleurisy just described, it may be associated with 
emphysema and chronic phthisis, or it may occur by itself. 

After death the pulmonary and costal pleura are found thickened and 
joined together by numerous adhesions. These changes may involve 
only a part or the whole of the pleura on one or both sides of the chest. 

The thickened pleura is covered with mesothelium ; the new connec- 
tive tissue may be very dense and may contain few or many cells. 
Blood-vessels may be numerous and irregular in distribution or few in 
number. 

Tuberculous Pleuritis. — Tuberculosis of the pleura is usually secondary 
to tuberculous inflammation elsewhere in the body, either in the lungs, 
which is most common, or the bronchial lymph -nodes, peritoneum, bones, 
etc. , or it may be a part of a general miliary tuberculosis. ^ There may 
be localized or widely disseminated miliary tubercles upon or beneath the 
pleural surfaces, either in direct association with lesions beneath the 
pulmonary pleura or apart from these or upon the costal pleura. The 
tuberculous foci may be larger and more diffuse. The minute chara ters 
of the inflammation are not essentially different from those found in 
tuberculosis in connective tissue elsewhere, but the mesothelial cells cov- 
ering the pleura may share largely in the early phases of the new growth. 

If the process be prolonged, much dense fibrous tissue may be formed 
in which are miliary tubercles in various stages of coagulation necrosis 
or larger patches of necrotic tissue surrounded by miliary tubercles or 
diffuse tuberculous tissue. 

With all types of tuberculous inflammation of the pleura more or less 
exudate may form. This may be sero- fibrinous, often with very little 
fibrin, or, as is frequently the case, it is tinged or deeply colored with 

^ Consult for cases bibliography Gordinier and Lartigau. Am. Jour. Med. Sciences, 
vol. cxxi., p. 43, 1901. 

'^ Netter, Bouchard and Brissaud's "Traite de Medecine," t. vii., p. 445, 1901. For 
a study of the ways of infection of the pleura see Grober, Deutsches Arch. f. klin. Med., 
Bd. Ixviii., p. 296, 1900, bibliography. 

3 For evidence of the frequency of primary tuberculosis of the pleura, consult 
Hodenpyl, New York Medical Record, June 24, 1899. 



THE EESPIEATOEY SYSTEM. 437 

blood. The exudate may be purulent. The tubercle bacillus may be 
associated with other bacteria, most often with the Staphylococcus pyo- 
genes in the purulent exudate. 

Many cases of pleuritis with a sero -fibrinous exudate giving no growth 
of bacteria on the ordinary culture media are found to be tuberculous, by 
the inoculation of guinea-pigs with the fluid. 



TUMORS. 

Fibroma, sarcoma, and endothelioma may occur as primary tumors of 
the pleura. Fibroma and lipoma formed in the subpleural tissues may 
encroach upon the pleural cavity. Endothelioma usually occurs in the 
form of larger and smaller, flat or projecting, irregular nodular masses 




Fig. 234.— Endothelioma of the Pleura. 
The inner surface of a segment of the costal pleura, containing three of the ribs, is shown in the cut. 

(Fig. 234), frequently most marked and extensive upon the costal pleura. ' 
This as well as other tumors of the pleura may be associated with an 
exudative pleuritis. 

Carcinoma, primary in the thyroid, mamma, oesophagus, and stomach, 
may invade the pleura. Small white, slightly projecting, often pig- 
mented elevations of the pleura, either single or multiple, are common. 
These were formerly regarded as mostly miliary fibromata. But Hoden- 
pyl and others have shown that while some may be fibromata or lym- 
phangiomata or air cysts, they are mostly fibrous masses which replace 
or enclose miliary tubercles. Echinococcus and other cysts of the pleura 
have been recorded. ^ 

^ For bibliography of endothelioma of the pleura consult Glockner, Zeits. f . Heil- 
kunde, Bd. xviii., p. 209, 1897. 

■^For a description of ciliated cysts of the pleura, see ZaJin, Virchow's Arch., Bd. 
cxliii., p. 17i. 



438 THE RESPIRATORY SYSTEM. 

The Lungs and Bronchi. 
The Bronchi. 

HAEMORRHAGE. 

In haemorrhage from the bronchi the source of the blood is often to 
be sought in the parenchyma of the lung (see page 445) or in a ruptured 
aneurism. But haemorrhage from the bronchial walls may occur in 
tuberculous or other forms of ulceration, chronic bronchitis, malignant 
tumors, etc. 

INFLAMMATION. (Bronchitis.) 

Acute Catarrhal Bronchitis. — This is frequently associated with a simi- 
lar process in the trachea. It is characterized by hypersemia and swelling 
of the mucous membrane with the formation of exudate, which usually 
consists largely of mucus formed by the hypersecretion of the mucous 
glands or degeneration of the epithelial cells. Mingled with this are 
exfoliated and more or less degenerated epithelium from the mucous 
membrane, leucocytes from the dilated vessels of the submucosa, varying 
numbers of red blood cells, and bacteria. 

The microscopic appearances differ in different parts of the bronchial 
tubes in accordance with the differences in structure. Mucous glands, 
when these are present, may reveal great functional activity, and their 
ducts may be distended with mucus which, often mingled with exfoli- 
ated and degenerated cells, streams out upon the surface. Swelling and 
proliferation of the connective-tissue cells and endothelium of the vessels 
of the submucosa, oedema, and emigration from the dilated vessels are 
often marked. The leucocytes may be seen making their way through 
the epithelium into the other exudates upon the surface. The epithelium 
may be loosened, single or clustered cells falling off here and there, or 
shreds of cells may exfoliate together (see Fig. 235). The deeper sphe- 
roidal epithelia, the so-called mother cells from which the new ciliated 
cells on the surface are formed in both physiological and pathological 
regeneration, usually remain in place upon the basal membrane. In the 
small bronchi whose walls are thin, little else may be seen than an irreg- 
ular exfoliation of the epithelium. On the other hand, the smaller 
bronchi may be much involved and their lumina filled with exudate ; 
when this, which has been called "capillary bronchitis, ^^ occurs, the 
inflammatory process usually involves the adjacent and associated terri- 
tories of lung tissue, constituting one of the important forms of broncho- 
pneumonia. In some forms of bronchitis the exudate may consist 
largely of pus. 

Atelectasis of corresponding tracts of the lung may follow the occlu- 
sion of the bronchi with exudate. As recovery advances, the submu- 



THE RESPIRATORY SYSTEM. 439 

cosa assumes its normal thickness and character and the epithelium is 
regenerated from the cells of the deeper layers. 

Various forms of bacteria may be associated with acute bronchitis, and 
are presumably the excitants under favorable conditions of the lesions ; 
the etiological relationship has, however, not yet been experimentally 
established. The most common forms of bacteria are Streptococcus pyo- 
genes, the pneumococcus, Staphylococcus aureus, and the influenza 
bacil] us. ' 

Chronic Catarrhal Bronchitis. — This form of bronchitis may be the sequel 
of one or more attacks of acute bronchitis. More frequently it is associ- 
ated with emphysema, heart disease, interstitial pneumonia, phthisis, 




Fig. 235,— Acute Catarrhal Bronchitis. 

TMs section of a small portion of the bronchial wall shows considerable exfoliation of the epithelium, 
but many of the deeper so-called "mother cells "remain in place. There are swelling of the connective- 
tissue cells and congestion of blood-vessels in the submucosa, with oedema and emigration of leucocytes. 
Some of the leucocytes are passing through the epitheUum to mingle with the mucous exudate and exfoli- 
ated cells in the lumen of the bronchus. Some of the ciliated cells show the '" beaker " shape with a homo- 
geneous interior indicating the production of mucus within them. 

pleuritic adhesions, or the inhalation of irritating substances. There is 
in most cases a constant production of mucus, pus, and serum in consid- 
erable quantities, and these inflammatory products may have a very foul 
odor. Less frequently these products are very scanty — dry catarrh. 
The epithelium is deformed and desquamating, with a production of new 
cells in the deeper layers. There may be epithelial hyperplasia or atro- 
phy ; the mucous glands are large or atrophied ; there may be hyperpla- 
sia or atrophy of the submucosa ; the muscularis may be thickened or 
atrophied. These changes in the fibrous and muscular elements of the 
walls lead to the so-called ^^trabeculation" of their inner surfaces (Fig. 
236). Obliterating arteritis of the associated vessels may occur. These 
changes in the walls of the bronchi may lead to bronchiectasia. 

' For a study of the bacteria found in bronchitis see Ritchie, Jour. Path, and Bact., 
vol. vii., p. 1, 1900; also reference to bacteria in lungs, p. 459. 



440 



THE RESPIEATOEY SYSTEM. 



Acute Pseudo-membranous Bronchitis — Croupous Bronchitis — may occur 
with croupous laryngitis, as a lesion of diphtheria, with lobar pneumo- 




■•^ 



f 



A ^ 



<5. 



V . ^.-c- 



Fig. 



-Chronic Bronchitis with Moderate Bronchiectasia. 



This transverse section of a portion of the wall of a dilated bronchus shows atrophy of the epithelium; 
fibrous hyperplasia of the submucosa with the formation of longitudinal ridges on the interior of the tube 
(cut across in this section) ; thickening of the wall of the bronchus and atrophy of the mucous glands. 



nia, and sometimes without these associations. The bronchi are lined or 

filled with a mass of fibrin, j)us, and desquamated epithelium. Fibrin 

and pus may also be found beneath the epithelium and infiltrated in the 

stroma. 

Chronic Fibrinous Bronchitis is attended with the formation in one or 

more bronchi of masses of fibrin which are expectorated by the patient 

in the form of branching casts 
of the bronchi (Fig. 237). 
After death the bronchi are 
said to be but little altered 
from the normal. " 

Curschmann has described 
under the name '^bronchiolitis 
exudativa " a form of bron- 
chitis in which small threads 
and bands of gray or yellow, 
X^artly transparent, coagulated 
material are formed in the 
small bronchi — ' ' Curschmann ' s 
spirals.'^ These sometimes oc- 
cur in pneumonia. In different 
forms of bronchitis, especially 
in those associated with asth- 
ma, the exudation may con- 
tain small, octahedral bodies, 

probably comiDOsed of mucin. They are accidental formations, probably 

formed from cells, and may be found in the sputa. 

iFor bibliograph}^ see Fefzer, Deutsches Arch. f. kliu. Med., Bd. Ixvii., p. 337, 1900. 




Fig. 237.— Chronic Fibrinous Bronchitis. 

Fibrinous casts of the bronchi, similar to those shown 
in the photograph, were coughed up at irregular in- 
tervals for several years. 



THE RESPIRATORY SYSTEM. 



441 



BRONCHIECTASIA. 

Dilatations of the bronchi maybe cylindrical, fusiform, or sacculated. 
The sacculated dilatations are usually the larger. These communicate 
with one side of the bronchus. The peripheral iDortion of the bronchus 
may be obliterated ; the bronchus leading to the cavity may be of normal 
size, or dilated, or stenosed, or even completely obliterated. Such sac- 
culated dilatations may reach a very large size and may communicate 
with each other. Dilatations are apt to occur under conditions which 
interfere with the integrity of the bronchial wall. 

In acute general bronchitis and broncho-pneumonia in children, 



.y^^" 





^s^ a 



tu^^K. 



..rff^t^^-rg^ 



(i^^^ 



^7/ rQ ^ 



^yh'^' ' 














<? p 




Primary Adenoma of the Bronchi. 



cylindrical dilatation of a number of the medium -sized bronchi often 
occurs. 

In the persistent broncho -pneumonia of children such dilatations may 
reach a still greater development. Chronic bronchitis may lead to cylin- 
drical or sacculated dilatations, sometimes of great size. 

Occlusion of some of the bronchi, consolidation of portions of the 
lung, and extensive pleuritic adhesions may also lead to bronchiectasia. 

The walls of bronchiectatic cavities may be lined with mucous mem- 
brane, which, however, is apt to undergo various changes as the process 
advances. Thus the subepithelial layer may be vascular and cellular 
and thrown into folds, or it may be thin and dense. The epithelium is 
often irregular, sometimes irregularly thickened, sometimes thin, or it 
may be largely absent. The glands, muscle, and cartilages of the walls 
of the bronchi may disappear through atrophy. The presence of certain 
forms of bacteria in the exudate in bronchiectasia may lead to offensive 
putrefactive process and even to gangrene. 



442 



THE EESPIHATORY SYSTEM. 



In acute and chronic phthisis the tuberculous inflammation of the 
walls of the bronchi often gives rise to sacculated dilatations, which 
expand with time and become still larger by the destruction of the adja- 
cent lung tissue — tuberculous bronchiectasise. 



TUMORS. 

Primary tumors of the bronchi are rare. Lipoma, chondroma, and 
fibroma have seen observed. Sarcoma is rare, but may occur, especially 
in spheroidal cell forms, or as an extension of similar growths in the 
mediastinum. Adenoma (Fig. 238) and primary carcinoma are rare. 
Secondary carcinoma is not uncommon and may also involve the trachea 
of the lungs. 

In chronic bronchitis, polypoid hyperplasiae, simulating tumors, may 
project into the lumen. Ossification of the bronchial walls is of occa- 
sional occurrence. 



LESIONS OF THE TRACHEAL AND BRONCHIAL LYMPH-NODES. 



The tracheal and bronchial lymph-nodes may be the seat of a variety 
of lesions which, owing to their situation, as well as for other reasons, 

are of considerable practical impor- 
tance. They may be enlarged from 
hyperplasia in acute infectious dis- 
eases ; by the development in them of 
tumors; in leuksemia and with es- 
pecial frequency in tuberculosis (Plate 
III.). They may become pigmented 
from inhaled coal or other dust and 
may atrophy or become fibrous or 
calcified. In cheesy degeneration fol- 
lowing tuberculosis (Fig. 239), or in 
suppurative inflammation, perfora- 
tion may take place into the air 
passages, or the pulmonary blood- 
vessels, or aorta, or into the pericar- 
dial or pleural cavities; in this Avay 
haemorrhage or secondary inflamma- 
tory processes or gangrene may occur. 
Death may occur from pressure u\)on 
the trachea by tumors of the adja- 
cent lymph-nodes. Sudden death 
from asphyxia may result from per- 
FiG. 239.— Tuberculous and Caseous bron- foration into the trachea. Pressure 
cHiAL LYMPH-NODES. ^^^^^^ ^^^ pulmouary veins may lead 

The nodes are much enlarpred and press upon , ^ -, rr\i •, ^ ^t.-:„i 

the larger bronchi. to jDulmouary oedema. The bronchial 




PsXhology—Delafield and Prudden. 



Plate III, 




Tuberculous Bronchial Lymph-Nodes. 

The nodes are enlarged and caseous, with areas of commencing softening. An isolated 
tubercle in the lung tissue above the enlarged nodes indicates a local dispersion of the 
tubercle bacilli. The lung was hardened in alcohol. 



THE RESPIRATORY SYSTEM. 443 

lymph-nodes are very important as distributing centres of infectious 
micro-organisms, and particularly as points of lodgment of tubercle ba- 
cilli, which have been gathered from the pulmonary air spaces from the 
pharynx or elsewhere. ' 

The Lungs. 

Malformations. 

One or both lungs may be wanting or only partially developed. One lung is some- 
times converted into a number of sacs formed of dilated bronchi, while the lung paren- 
chyma is undeveloped. 

The lobes may be subdivided by deep fissures, accessory lobes may be present, or 
an accessory lung may be present. An accessory lung in the abdominal cavity has been 
described.'' There may be with absence of part of the wall of the thorax hernia of the 
lung. There may be transposition of the lungs, with similar changes in the position of 
the heart and the abdominal viscera. 



INJURIES— PERFORATIONS. 

Severe contusions of the thorax may produce rupture of the lungs, 
with extravasations of blood into the pleural cavities. 

The lungs may be wounded by a fractured rib and by penetrating 
weapons and projectiles. Such injuries often lead to bleeding into the 
lung tissue followed by inflammatory changes. The lungs, however, 
exhibit a considerable degree of tolerance for such injuries. 

Collections of pus in the pleural cavities, the mediastinum, the liver, 
the spleen, the kidneys, and the peritonal cavity may perforate the lungs. 
See also Hydropneumothorax. 



DISTURBANCES OF CIRCULATION. 

Anaemia. — The lungs may be anaemic in connection with a general 
anaemia of the body ; or from compression of a part or a whole organ, as 
by pleural exudates, tumors, or new-formed fibrous tissue ; from occlu- 
sions of blood-vessels or in atrophy of these in emphysema. 

Hyperemia ajs^d (Edema. 

Hypersemia may occur as the result of the inspiration of irritating 
gases ; from the presence of toxic substances in the blood ; in early phases 
of inflammation, or as the result of such an occlusion of vessels in one 
part as causes its accumulation in another. 

On the other hand, hypersemia of the lung is often due either to some 

^ Consult for summary of lesions of bronchial lymph-nodes Hall, Philadelphia Medi- 
cal Journal, December 1st, 1900, bibliography. See also concerning tuberculosis refer- 
ence Sorthrnp and Bovaird, p. 368. For an excellent resume concerning normal and 
pathological tracheal and bronchial lymph-nodes, see Marfan in Bouchard and Bris- 
saud's "Traite de Medecine," t. vii., p. 525. 

-Consult Vogel, Virch. Arch., Bd. civ., p. 235, 1899, bibliography. 



444 THE RESPIRATORY SYSTEM. 

hindrance to the exit of blood through the pulmonary vein, such as mi- 
tral stenosis or insufficiency, or to enfeeblement of the ventricular con- 
tractions, as in fatty degeneration of the heart muscle or interstitial myo- 
carditis. In the last hours of life the feeble action of the heart disposes 
to iDulmonary congestion. The position of the body upon the back in 
bed favors an accumulation of blood in the posterior portions of the 
lungs — hypostatic coiigestion. Hypersemic lungs are in varying degrees 
darker and heavier than normal ; an unusual amount of blood flows from 
the cut surface. CEdematous fluid is often also present. Eed blood 
cells often pass through the capillary walls in hypersemia and these with 
more or less exfoliated epithelium may be found in the air vesicles. 






*» ^ 







Fig. 340.— Chronic Congestion of the Lung. (Brown Induration.) 

Showing dilated capillaries of the walls of the air vesicles and haematogenous pigment in the exfoliated 

epithelial cells of the air vesicles. 

Chronic Congestion, — In prolonged hypersemia of the lungs, notably in 
connection with lesions of the mitral and aortic valve, or degeneration 
or dilatation of the left ventricle, the veins and capillaries, especially 
the capillaries, become permanently distended, pouched, and elongated, 
so that they often stretch in loops into the air spaces (Fig. 240). Eed 
blood cells find their way from the contorted vessels by diapedesis or small 
haemorrhages into the air vesicles or interstitial tissue of the lung. Here 
decomposition of the hsemoglobin leaves brownish pigment particles which 
may remain free or be taken into cells. In the air vesicles the epithelial 
cells usually desquamate in considerable numbers, and take up the 
pigment in varying amount. This i)igment gives to the lungs a peculiar 
brownish pink or salmon color. The appearance of these lungs may be 
modified by hsemorrhagic infarctions, by pre-existing emphysema or 
oedema, or by exudative inflammation. Associated with these changes 



THE EESPIEATOEY SYSTE3I. 445 

there is usnally a new formation of fibrous tissue, so that the lung be- 
comes indurated, leathery, and dry, and collapses less readily than nor- 
mal. This condition is often called hroicn induration of the lung. This 
formation of fibrous tissue is analogous with that which occurs in other 
organs, such as the kidney and liver in chronic congestion. Emigration 
of leucocytes is not infreciuently associated with diapedesis from the 
dilated cai^illaries, and these, with the desquamated epithelium, may 
accumulate in the air vesicles. 

In oedema of the lungs the vesicles contain a clear, sometimes foamy, 
fluid, occasionally tinged with blood, usually mixed with exfoliated ves- 
ical epithelium. The oedematous fluid may be present in the bronchi 
and in the interstitial tissue of the lungs, ffidema is often associated 
with hyperaemia, and like this may vary in different parts of the lung. 
On the other hand, there may be extensive oedema without overfilled 
blood-vessels ; these in excessive oedema may indeed be nearly empty and 
comi^ressed. CEdema of the lungs may occur in general infections and 
intoxications, or in association with local inflammatory processes. Fatal 
oedema of the lungs may be associated with fat embolism. 

The studies of Welch ' show that with diminished force exerted by 
the left side of the heart, the vigor of the right remaining unimpaired, 
oedema of the lungs may follow. ^ 



HEMORRHAGE AND INFARCTION. 
HEMORRHAGE. 

Haemorrhages into the lung tissue and air spaces of the lungs may 
occur from trauma, from rupture of aneurism, in acute infectious dis- 
eases and intoxications, in scurvy and hsematophilia, in asphyxia from 
brain lesions or other conditions, from tuberculous ulcerations involving 
the blood-vessels. Multiple ecchymoses may occur in fat embolism. 

Haemorrhage is of frequent occurrence in excessive hyperaemia of the 
lungs, notably in connection with mitral stenosis and insufficiency. Un- 
der these conditions the extravasation of blood may take place by diape- 
desis or by rhexis. The accumulations of blood may be single or mul- 
tiple, localized or diffuse, dense and firm, or when oedema is present, 
soft and fluid in character. During the last hours of life, owing to en- 
feeblement of the heart, extravasation of blood may occur which sinks 
to the posterior dependent i)ortions of the lungs. 

IXFAECTION. 

As a result of thrombosis or embolism of the pulmonary artery, dense 
collections of extravasated blood may form, called Jicemorrhagic infarc- 

^ WelcJi, Yirchow's Arcliiv, Bd. Ixxii., p. 375. 

- For a study of the disturbances of circulation in the lungs under various abnormal 
conditions see A^?-, Centralbl. f. ges. Med., January 26th, 1901, bibliography. 



446 THE RESPIRATORY SYSTEM. 

tions. These infarctions are often multiple, usually circumscribed, and 
rounded or wedge-shaped, from the size of a walnut to that of an orange. 
They are of dark -red color, hard and unaerated, with the air spaces 
distended with blood, and are often surrounded by a zone of inflamma- 
tory exudate. They may be situated in any part of the lungs, but are 
most common in the lower lobes. At the apices of the infarction, the oc- 
cluding thrombus or embolus may be discovered. When, as is usually 
the case, they are near the surface of the lungs, a circumscribed inflam- 
mation of the pleura often occurs. 

Such infarctions may be followed by death ; they may become gan- 
grenous, or if the emboli or thrombi be not infectious, the blood may 
become absorbed, and, especially in the smaller forms which are more 
often due to embolism, they may be gradually changed into a smaller 
mass of pigmented fibrous tissue. 

A large part of the lungs may be involved in haemorrhage due to 
thrombosis of large trunks of the pulmonary artery. ' Hsemorrhagic in- 
farctions from thrombosis or embolism are most frequent in lungs which 
are the seat of chronic congestion. The most common source of the em- 
boli of the pulmonary artery is the right heart or peripheral thrombi. ' 



ATELECTASIS. 

In atelectasis the walls of the air spaces lie together, either because 
they are collapsed or compressed, or because, as in congenital atelectasis, 
the lungs, or portions of them, have not been expanded in respiration. 

In foetal or congenital atelectasis defects in the respiratory mechanism, 
or blocking of the air passages, may be responsible for the unaerated 
condition which may affect only parts of a lung or a whole organ. The 
atelectatic portions of the lungs are dark red in color and of fleshy con- 
sistency." 

Atelectasis may, on the other hand, be acquired, either in childhood 
or in adult life. In young children collapse of portions of the lung is 
of frequent occurrence, through occlusion of bronchi by inflammatory 
exudate. The region thus cut off' is gradually deprived of air, so that 
as the blood continues to circulate, it is dark red and firm in texture. 
Compression atelectasis may be dueto exudates, tumors, etc., in the pleu- 
ral cavities. Under these conditions the portion of lung involved may 
be paler than normal from the pressing out of the blood. In adults, 
large or small portions of lung tissue may collapse from occlusion of 
a bronchus by exudate or stenosis, by paralysis of the vagus, or in long- 
continued feebleness of respiration. Oedema may be associated with 
collapse. 

Atelectasis may resolve by an early admission of air to the collapsed 

' For a fuller consideration of embolism and thrombosis of the pulmonary artery 
consult Welch, in Allbutt's "System of Medicine," vol. vi., p. 261. 

■^ Collapsed lungs from their red color and fleshy consistency are often spoken of as 
"carnified." 



THE RESPIRATORY SYSTEM. 



447 



regioD. On the other hand, if prolonged, fibrons tissue may form and 
the involved portion may be finally converted into a cicatricial mass, 
sometimes containing bronchiectatic cavities. 



EMPHYSEMA. 

Vesicular Emphysema. — In forcible inspiration or expiration through 
obstruction of the air i^assages, in coughing, or in the use of wind instru- 
ments, or with consolidation or compression of portions of the lungs, the 
walls of the air spaces of the lungs may be more or less distended, either 
in circumscribed regions or over large areas of the lungs. This may de- 




Fig. 241.— Vesicular Emphysema. 
Showing enlargement of the air spaces and thinning of their walls. 



velop in a short time, and then the condition is designated acute emphy- 
sema. 

If the conditions which induce emphysema be persistent, as in chronic 
bronchitis with difficult respiration and coughing, atrophy of the walls 
of the air vesicles and alveolar passages may take place — chronic emphy- 
sema. The walls become thinner and are often perforated; adjacent air 
spaces coalesce, so that larger and smaller irregular, thin-walled cavities 
are formed (Fig. 241). Destruction of the capillary network of the 
atrophied walls occurs, and the lung may thus become i)ale and anaemic. 
As a rule, the distention of the air spaces is most marked along the an- 
terior margins of the lungs, but it may be more general. Through the 
atrophy of the elastic tissue of the lungs, when the lesion is general and 
advanced, these organs do not collapse when the chest is opened. They 
appear pale, are dry and soft, and pit on jiressure by the finger. 

The microscopic picture is that of varying degrees of atrophy ; des- 
quamation and fatty degeneration of the vesical epithelium are common. 



448 THE RESPIRATORY SYSTEM. 

As already indicated, emphysema of the lungs is often associated with 
chronic bronchitis. With this may be more or less hyperplasia of the 
interstitial tissue. Dilatation or hypertrophy of the wall of the right 
ventricle is common. Chronic endarteritis of the pulmonary vessels may 
be associated with emphysema. There may be chronic venous conges- 
tion of the abdominal viscera and dropsy. Delafield holds that the more 
essential lesion in some forms of emphysema is the development of new 
connective tissue with which dilatation of the air vesicles and atrophy 
of their walls are in varying degrees associated. 

In old age, atrophic processes in the lungs may be associated with 
dilatation and mergence of the air spaces. This is called senile emphy- 
sema. 

Interstitial Emphysema. — Eupture of the walls of the air spaces may 
permit the escape of air into the interstitial tissue of the lungs. Eup- 
ture of the pulmonary pleura may admit air into the mediastinum and 
thence into the tissues of the neck. Gas may form after death in the 
interstitial tissue of the lungs from the presence of the Bacillus aerogenes 
capsulatus or other putrefactive bacteria. 



GANGRENE. 

Circumscribed gangrene occurs in the form of one or more rounded 
or irregular masses of variable size. The gangrenous portion of lung is 
at first brown and dry. The surronnding lung tissue is congested or 
cedematous, or infiltrated with blood, or inflamed. If the gangrenous 
focus is near the pleura, the latter will be coated with fibrin. Gradu- 
ally the gangrenous portion of lung assumes a dirty green color and a 
putrid odor. It becomes soft, disintegrated, and separated from the 
surrounding lung. The blood-vessels may be obliterated by thrombi, or 
eroded, so that there are profuse hsemorrhages. 

Such a gangrenous process may extend to the adjacent lung tissue, or 
a zone of gray or red hepatization or of connective tissue may be formed. 
The fluid from the gangrenous lung may pass into the bronchi and be 
expectorated ; or it may run from one bronchus into another and incite 
new gangrenous foci or diffuse gangrene. The pulmonary pleura may 
be perforated and a gangrenous pleurisy produced. Gangrene may fol- 
low lobar or broncho -pneumonia, especially such phases of the latter as 
result from the inspiration of foreign material containing micro-organ- 
isms from the mouth ; it may arise from infectious emboli in the lungs, 
or by an extension of a gangrenous process from an adjacent part. 

Diffuse gangrene may follow the circumscribed form ; it may compli- 
cate lobar pneumonia or occur as an independent condition. A large 
part of a lobe or of an entire lung becomes greenish, putrid, and soft, 
and the pulmonary pleura is inflamed. There may be haemorrhages from 
eroded vessels. There may be general septicaemia. 

Various forms of bacteria may be present in gangrenous areas of the 



THE EESPIEATORY SYSTEM. 449 

lungs. Among those frequently present is the Staphylococcus pyogenes, 
Streptococcus pyogenes, pneuniococcus, and various saprophytic micro- 
organisms. 

INFLAMMATION. (Pneumonia, Pneumonitis.) 
General Considerations. 

Before commencing the study of inflammation of the lungs it is well to recall some 
of those features of structure and function which influence the local manifestations of 
disease in these organs and largely determine the special character of its lesions. In 
the first place, the lungs, like the gastro-intestinal canal, while in a topographic sense 
within the body, are still in open communication w^ith the exterior, and are thus more 
directly exposed to various deleterious agencies than are those structures and organs 
wholly enclosed by living tissues. Notwithstanding this vulnerability of location, the 
recesses of the lungs are guarded by protective mechanisms of great eflHciency. Thus 
in normal respiration the air, which often bears as dust many organic and inorganic 
substances as well as minute living organisms, is largely cleansed by its repeated im- 
pingement upon the moist mucous surfaces of the nose, pharynx, larynx, and bronchi. 
The ciliated cells of these membranes are constantly sweeping upward such of these 
particles as have lodged upon them, while by the lymph channels and the lymph-nodes 
foreign substances which have escaped the barriers are either removed or stored in the 
least harmful situations. Damage to the integrity or efficiency of these jDrotective 
agencies is a factor in the origin of pulmonary diseases too often ignored. 

The responses of the lung tissues to the excitants of inflammation are not funda- 
mentally as distinct nor as variable as the common classifications of pneumonia would 
seem to indicate. Exudation from the smaller blood-vessels is one of the most common 
features of the acute phases of pulmonary inflammation. 

The formation of exudates is favored by the extensive capillar}^ network which is 
almost directly exposed to such deleterious agents as may gain access to the air spaces ; 
while a great accumulation of exudates is possible owing to the spongy structure of 
the organs. 

The transitional character of the epithelium lining the air vesicles predisposes to 
cell proliferation and exfoliation, and thus to the formation of exudate. 

On the other hand, the abundant blood and lymph channels^ favor the speedy re- 
moval from the air spaces in the lungs of large quantities of exudate. 

While the abundant lymphatics of the lungs aid in the rapid disposal of exudates, 
they, on the other hand, favor the absorption of toxic substances into the body at large 
when bacteria, for example, are the excitants of the local inflammation.'-' So that al- 
though exudative pneumonia is commonly considered a local disease, it is often rather a 
local expression of a general infection or is doubly significant on account of the asso- 
ciated toxaemia. 

In addition to the development and accumulation of exudates, necroses and the 
formation of fibrous tissue are the most notew^orthy general pathological processes in 
the lungs. 

While the conspicuous differences in the various forms of pneumonia are largely 
due to differences in the nature, virulence, and distribution of their excitants, predis- 
posing factors dependent upon age, constitutional condition, and the protective mechan- 
ism of the lungs are of great significance. 

The common classifications are based partly upon etiology, partly upon morphol- 
ogy, and the names used suggest now the topography of the lesions or the character of 
the tissue which is especially affected, and again the species of the bacterial excitant. 
Thus the term lobar pneumonia is topographical ; tuberculous pneumonia emphasizes 
the excitant ; while interstitial pneumonia suggests the form of tissue involved. 

' See Miller, Arch. f. Anat. und Physiologic, Anat. Abth., 1900, p. 197, bibliography. 
'Xote by CJonncilman, "The Lobule of the Lung and its Relation to the Lym- 
phatics," Boston .Jour. Med. Sciences, vol. iv., p. 165, 1900. 
29 



450 THE RESPIRATORY SYSTEM. 



Acute Lobar Pneumonia. (Fibrinous Pjieamonia— Croupous 

Pneumonia. ) 

This is an infectious disease incited by the Micrococcus lanceolatus 
(pneumococcus of Fraenkel).' It is especially characterized by an exu- 
dative inflammation in which red and white blood cells, serum, and fibrin 
accumulate in the air spaces of the lungs, usually involving, especially in 




Jv% 






riG. 243.— Acute Lobar Pneumonia— Early Stage. 

This single air vesicle shows congestion of the capillaries in the walls, and a small amount of exudates, 
fibrin, leucocytes, red blood cells, and exfoliated epithelium. 

adults, the whole of one lobe or lung or portions of both lungs. ^ Toxae- 
mia from the absorption of i)oisons formed locally in the lungs is an 
important and often most significant factor in the disease. The pneumo- 
coccus is occasionally widely disseminated in the blood. 

During the first hours of the inflammation the capillaries of the air 
spaces are congested, the lung is oedematous, firmer than normal, but not 
markedly consolidated. The air spaces contain varying numbers of leu- 
cocytes, red blood cells, serum, and fibrin (Fig. 242). The epithelial 
cells lining the air vesicles may be swollen, they sometimes proliferate, 
and are usually detached in considerable numbers. Catarrhal bronchitis 
and iDleuritis may at this time develop. This is called the stage of ^^con- 

' We shall use liere as synonymous the names Micrococcus lanceolatus and pneumo- 
coccus ; when pneumococcus is used the pneumococcus of Fraenkel is referred to. For 
a description of this organism, see p. 191. 

^ Tlie clinical course and the morphological characters of the inflammation of the 
lungs associated with the Micrococcus lanceolatus are so typical that we seem justified 
in limiting the term lobar or fibrinous pneumonia to this condition, even though inflam- 
mations of the lungs due to other excitants are occasionally lobar in extent and may 
have a fibrinous exudate, and though exceptionally the pneumococcus inflammation 
itself fails to reach lobar proportions. 



THE RESPIRATORY SYSTEM. 451 

gestion^^ or ^^engorgement" and may last for a few hours or for several 
days. 

As the process continues red blood cells, bnt especially polymorpho- 
nuclear leucocytes, and fibrin accumulate in the air si)aces and smaller 
bronchi, so that the portion of lung involved becomes solid and friable, 
somewhat resembling the liver in color and consistency; hence the term 
'^ red hepatization " which has been used to indicate this condition. The 
cut surface of the consolidated portion is dry and coarsely granular, the 
granules being plugs or casts of exudate in the air spaces. A light 
scraping of the cut surface of the lung with the knife readily removes 
these granules or plugs of exudate, which consist largely of fibrin and 
leucocj^tes with red blood cells and exfoliated epithelium (Fig. 243). 
The relative amount of leucocytes, red blood cells, and fibrin in the air 
spaces varies greatly, sometimes one, sometimes the other, preponderat- 
ing. The fibrin fibrils often coalesce or swell, forming homogeneous, 
irregular masses. On staining, large numbers of pneumococci may be 
found mingled with the other elements. While the general appearance 
of the lung in this stage is red, it is often mottled with gray and fre- 
quently is not uniformly solid. Although the capillary blood-vessels are 
compressed, they for the most part remain pervious ; but thrombosis is 




Fig. 243.— Acute Lobar Pnefmonia— Stage of "Red Hepatization." 

The air vesicles are fllled with exudate consisting largely of leucocytes, fibrin, and serum with a few epithe- 
lial cells. 

not infrequent. Fibrinous x)leuritis is commonly jDresent and the inter- 
stitial tissue of the lung, while usually free from exudate, may be oedem- 
atous and contain a few leucocytes and some fibrin. 

The quantity of exudate in the lung is often very large. Hodenpyl 
has found it sometimes to be from three to four or even six pounds in 
weight. 

In the usual course of events the red blood cells now lose their haemo- 
globin, the exudate begins to soften, and the lung assumes a grayish 



452 THE RESPIRATORY SYSTEM. 

color — gray hepatization or commencing resolution. The leucocytes and ex- 
foliated, epithelium undergo granular and fatty degeneration or necrosis, 
and these with the fibrin soften and disintegrate (Fig. 244). The cut 
surface of the lung is now moister, less granular, and is often covered 
with a grumous fluid. The softened exudate is gradually absorbed or 
may be in part expectorated. The involved portion of lung again con- 
tains air, the epithelium of the air spaces is regenerated. ^ 

While it is customary and convenient to describe definite stages of 
lobar inflammation of the lung — red and gray hepatization and resolu- 
tion — these in fact not only merge 
- ^ gradually into each other, but 

' _. , #^i often coexist in different parts of 

^^^ ;' .^# *^ f^ ^^^ lung. The process of repara- 

^' n ^J^:. y"'-'f'! tion also usually occurs irregularly, 

■ ^-) so that a lung in resolution may 

'' show side by side in neighboring 

air spaces well -formed cellular and 
fibrinous exudate, degenerated exu- 
date, and various phases of epithe- 
lial cell repair. 

Associated Lesions in Other Or- 
gans. — Fibrinous or sero- fibrinous 
FIG. 244.-EXUDATE FROM THE LuNtt IN resolt- plcuritis, usually wltfi sllght but 



§ 




ING LOBAR PNEUMONIA. ^^^^^^ ^-^j^ VOlumiuOUS CX 

The cells Show various phases of granular and commonly aCCOmpauicS lobar 
fatty degeneration with fragmentation of the nu- ^ ^ 

del and disintegration of the cell bodies. monia. Catarrhal and fibril 

bronchitis is also usually associate 
with the j)neumonic process. Pericarditis and endocarditis are not in- 
frequent complications ; meningitis occasionally occurs. The excitant 
of these complications is usually the pneumococcus. 

Chromatolysis of the ganglion cells, albuminous degeneration in the 
kidney, liver, and heart, hyperi)lasia of the bronchial lymph-nodes, to- 
gether with leucocytosis, fever, and frequent serious enfeeblement of the 
heart action are marks of toxaemia. The bronchial lymph-nodes may 
contain, especially in the perifollicular sinuses, and often within phago- 
cytes, red blood cells, cell detritus, and pneumococci brought from the 
lungs; fibrin is frequently also present. 

In lobar pneumonia in young children, in those enfeebled by acute 
and chronic disease, and in the aged, the lungs are often less uniformly 
consolidated and less dense and hard than in vigorous adults. When 
lobar pneumonia occurs in lungs already the seat of chronic lesions, such 
as chronic congestion, emphysema, interstitial pneumonia, or tuberculo- 
sis, the gross appearances of the organs may differ in various ways from 
those of uncomplicated pneumonia. 

^ For a study of the histology of acute lobar pneumonia with bibliography see 
Pratt, Contr. to Welch Anniversary Volume, 1900, p. 265, and Johns Hopkins Hospital 
Reports, vol. ix. 



THE EESPIEATOEY SYSTEM. 



453 



While Micrococcus lanceolatus is the regular excitaut of lobar pueu- 
mouia, other bacteria — see below — are not infrequently associated with 
it, sometimes though by no means always leading to clinical comiDlica- 
tions and to modifications of the appearance of the lesion. Predisposi- 
tion of the individual is an uncommonly conspicuous and imi^ortant fac- 
tor in the etiology of this as other forms of pneumonia, so that, as is well 
known, exposure, fatigue, etc. , may induce the favoring bodily condi- 
tions under which the pneumococcus becomes harmful. The experiments 
ui)on animals are most conclusive in demonstrating that intrapulmonary 
injections of pneumococcus cultures, which may be entirely without ob- 
vious effects in a healthy animal, may induce exudative inflammation or 
become quickly fatal after such exposure to cold or fatigue or injury or 



Hv 









y 









Fig. 245.— '' Organizing " Pneumonia -Delayed Resolution After Lobar Pneumonia. 

Anastomosing fascicles of fusiform connective-tissue cells lie within the air vesicle and are continuous Avith 
similar new formations in adjacent air spaces. 

to the action of drugs, as interferes with the integrity of the blood or 
locally damages the pulmonary tissues. ' 

Delayed Resolution after Lobar Pneumonia ("Organizing Pneumonia"). 
— Instead of undergoing resolution, the fibrinous and cellular exudate in 
the air spaces in lobar pneumonia may persist and by a process similar 
to that which is called organization of a thrombus (page 73) may be 
gradually replaced by new vascular fibrous tissue. Xew connective-tis- 
sue cells grow out from the walls of the air spaces into the exudate ; these 
cells become elongated. Intercellular fibrils develop, and long masses 
or bands of this new tissue, often containing blood-vessels, may extend 
for considerable distances through the air channels of the lung (Fig. 
245). These may gradually coalesce with the walls, and together with 
an interstitial connective -tissue growth may lead to a fibrous consolida- 
tion of the lung. 



^ For reference to experimental excitation of pneumonia see p. 459. 



454 THE RESPIRATORY SYSTEM. 

Delafield describes such an intra- alveolar formation of connective tis- 
sue leading to fibrous induration of lobes of the lung and occurring as an 
independent lesion apart from the exudative form of lobar pneumonia. 



Concurrent Infection and Suppurative Inflammation of the 
Lung Following Lobar Pneumonia. 

Although as stated above Micrococcus lanceolatus usually occurs alone 
in typical lobar pneumonia, it may be accompanied by the Streptococcus 
and Staphylococcus pyogenes and occasionally by other micro-organisms. 
The exact significance of these mixed or concurrent infections in lobar 
pneumonia is not always clear. But instead of the usual resolution there 
may be gangrene ; or supi^uration of the interstitial lung tissue with the 
formation of abscess may occur. In such cases Streptococcus pyogenes 
and Staphylococcus pyogenes aureus or putrefactive bacteria may be 
present with the pneumococcus in the exudate. 

Suppurative inflammation of the interstitial tissue of the lungs may 
involve not only the larger fibrous-tissue bands but the walls of the air 
vesicles and other air spaces. It is often called '^purulent infiltration." 
From the cut surface of the lungs in resolving lobar pneumonia, a gru- 
mous fluid resembling pus often exudes, and this is sometimes mistaken 
for a mark of interstitial suppuration of the lung. 

Suppurative inflammation of the interstitial tissue of the lung may 
occur without association with lobar pneumonia. 

Lobular Pneumonia and Broncho -Pneumonia. 

In distinction from that common form of pulmonary inflammation 
induced by the Micrococcus lanceolatus, which as we have seen is usu- 
ally lobar in character, there are exudative inflammations of the lungs, 
due to many different excitants, which are ^^ patchy" or 'lobular " in 
extent, the consolidated areas varying in size from such as are scarcely 
visible to those several centimetres in diameter. ^ These patches of lobu- 
lar consolidation often join and merge, so that solidification of whole 
lobes or lungs is not uncommon. But the mottled, uneven surface and 
color of the lungs on section, and the usual absence of the peculiar granu- 
lation, ordinarily suffice for the distinction even to the naked eye of the 
lobar from the coalescent lobular forms of exudative pneumonia. 

It is convenient to recognize several types of lobular exudative pneu- 
monia, although the character of the exudate is not distinctive. 

^ The term lobular does not refer exclusively to the anatomical " lobule " of the lung, 
since the masses or patches of consolidation often embrace several lobules or parts of 
these. 



THE RESPIEATOHY SYSTEM. 



455 



Bronclio-Pneumonia.- 



-Lobular Pneumonia with Inflammation of the 
Smaller Bronchi. 



This most imi3ortant type of lobular pneumonia frequently develops 
in connection AYith and as an extension of that form of inflammation of 
the smaller bronchi commonly called ^^ capillary bronchitis.^' At first 
dark red in color, the lobular areas of consolidation in broncho-pneu- 
monia become more gray at the centre through degeneration of the ex- 
udate, while the advance of the process in the periphery is marked by 
a less solid, redder zone. On section of the fresh lung these areas (Fig. 
246) usually project somewhat above the general surface and at their cen- 




FiG. 246.— Broncho-Pneumonia in an Adult. 

Showing several areas of consolidation with the central bronchus filled with exudate— stained dark in the 
section from which the photograph was made. 



tres the involved bronchi may appear as lighter spots, from which pus 
may exude or be easily pressed out. Such areas may coalesce, forming 
larger consolidations. The exudate which more or less completely fills 
the air spaces (Fig. 247) consists of serum, old and new-formed epithe- 
lial cells from the walls of the air spaces, red blood cells, and often fibrin 
and polymorphonuclear leucocytes (Fig. 248) with various forms of 
micro-organisms. As a rule, however, fibrin and leucocytes are not as 
abundant as in the exudate of lobar pneumonia. Mucus and bronchial 
epithelium may be aspirated into the air spaces and mingled with the 
exudates. 

Broncho -pneumonia involves a direct extension of the inflammatory 
process from the bronchi to the contiguous lung tissue, so that there is 
both an interstitial and exudative i)neumonia about the bronchial tubes, 
the whole forming the lobular areas of consolidation (Fig. 249). This 



456 



THE RESPIRATORY SYSTEM. 



involvement of the bronchial wall in inflammation with a direct exten- 
sion of the process to the surrounding lung tissue has been urged espe- 




Fig. 247.— Broxcho-Pxeumonia ix a Child. 

The section sbows a single lobular area of consolldatlonwlth its bronchus whose thickened wall merges with 
the surrounding zone of exudative pneumonia. 



cially by Delafield as the process to which the term hronclw -pneumonia 
should be par excellence applied. 

Between the consolidated areas there may be atelectasis of lung tissue 
from the occlusion of the smaller bronchi with exudate. When the con- 
solidated areas are situated at the surface of the lungs, fibrinous pleuri- 
tis may be present over the atfected regions. 

This form of broncho-pneumonia is frequent in children, sometimes 
as an independent process, but often associated with or following diph- 
theria, scarlatina, measles, etc. It oc- 
curs also in adults, either as a compli- 
cation of infectious diseases such as 
tyj)hoid fever, smallpox, influenza, etc., 
or as a primary process. It may occur 
in the aged or those enfeebled by chronic 
wasting diseases. 

Eesolution may take place in the 
areas of broncho-pneumonia by proc- 
esses of cell degeneration and absorp- 
tion identical with those through which 
restoration is secured in lobar pneumo- 
nia. If, however, resolution in broncho- 
pneumonia do not presently take place 
and the lesion persist, dense connective 
tissue is apt to form about the bronchi and in the interstitial tissue of 
the lungs, which may lead to induration and distortion of the organs, 
atelectasis, chronic bronchitis with dilatation of the bronchi, etc. A 




Fig. 248. 



—Broxcho-Pneumoxia— Exudate 
IX A SixGLE Air Vesicle. 



THE RESPIRATORY SYSTEM. 457 

photograph of a section of such a chronic or ^^ persistent " broncho- 
pneumonia is reproduced in Fig. 250. 

Other Forms of Lobular and Broncho-Pneumonia. — There are forms or 
types of lobular pneumonia in which serum and epithelial cells with 
more or less fibrin and leucocytes collect in the air spaces of a limited 
region without primary bronchitis and without involvement of the walls 
of the bronchi and air spaces. 

In one type of lobular pneumonia and broncho -iDueumonia the exu- 
date may consist largely of pus cells which infiltrate the walls of the air 
spaces and bronchi as well as fill the air spaces themselves. This type 
of inflammation may be induced by the aspiration in feeble persons of 
irritating substances or bacteria -containing material of various kinds^ 

sji ( i 



.^'-^^sT".- \:rr/m4^\'' agfc£V?ts 



■' b 







Fig. 249.— Broncho-Pneumonia— Child. 

Showing slight change in the epithelum of the bronchus ; a purulent exudate in the lumen ; thickening of 
the wall of the small bronchus, and exudate in the adjacent air vesicles. 

particles of food, saliva, etc. This is called aspiration pneumonia and 
may result in necrotic or gangrenous processes in the involved regions 
of the bronchi and lungs. Again there may be circumscribed areas of 
exudative pneumonia, often suppurative in type and involving the walls 
of the air spaces, which originate through the transportation by the 
blood-vessels of various forms of bacteria, especially the Streptococcus 
and Staphylococcus pyogenes, as in pyaemia ; this is called lobular pneu- 
monia of Jicematogenous origin or pycemic pneumonia. Thus abscesses of the 
lungs may be formed. 

In the lobular pneumonia of bubonic plague the exudate is said to 
contain few leucocytes and epithelial cells and to consist largely of blood 
and plague bacilli. ^ 

In the aged or those long in bed in an enfeebled condition, hyperse- 

^ Consult Flexner, Trans. Assn. Am. Phys., vol. xvi., 1901. 



458 



THE RESPIRATORY SYSTEM. 



mia and oedema with more or less exudate, usually epithelial in charac- 
ter, may develop in the dependent posterior portions of the lungs — hy- 
postatic congestion and hypostatic pneumonia. 

There is a peculiar and rare form of broncho -pneumonia associated 
with necrosis in which forms of streptothrix have been isolated which 
are undoubtedly the excitants of the disease. ' Actinomyces is also an 
occasional excitant of broncho -pneumonia. 

In all these forms of lobular pneumonia oedema and atelectasis of 
uhinvolved portions of the lung may occur. 

It is evident that in lobular pneumonia the infectious agent may reach 
the lungs either through the air passages or through the blood or lymph 




Fig. 350.— Persistent— Chronic— Bronciio-Pneumonia. 



vessels, and that differences in the portals of entry as well as in the 
nature and virulence of the excitant and the susceptibility of the indi- 
vidual have an imi)ortant bearing both upon the course of the disease 
and the morphology of the lesion. 

The Excitan^ts of Lobular and Broncho -Pneumonia.— The 
excitants of broncho-pneumonia and other types of lobular pneumonia 
are most frequently Streptococcus pyogenes (Fig. 251), the pneumo- 
coccus, Staphylococcus pyogenes, the typhoid diphtheria, influenza, and 
plague bacilli, the pneumobacillus of Friedlander; the streptothrix 
above mentioned, and other bacteria have been occasionally found. 

^ Consult Norru and Larkin, Jour, of Exp. Med., vol. v., p. 155, 1900, bibliography 



THE EESPIKATORY SYSTEM. 



459 



Pathogenic moulds may be excitants of acute forms of lobular pulmonary 
inflammation. 

It will thus be seen that while it is convenient to group the exudative 
forms of pulmonary inflammation on the basis of distinctions which are 
in part morphological, in part etiological, the types in fact frequently 
merge or concur. This should not lead to confusion if we remember 
that these are infectious diseases whose most conspicuous lesion is located 
in the lungs, and that they are not species in the natural history sense, 
for which fixed and definite characters must be established, but that the 
groups only indicate various forms and phases of response of a living 
organ in various conditions of susceptibility to the damage inflicted by 
one or another, and not infrequently by two or more combined forms of 




1^'^ -.- -'^ ,^5"" ■■'•A ■ -^ - 











A V '^■^;/^ 






f >i 



if 



Fig. 251.— Air Vesicle in Broxcho-Pneumonia with Streptococci. 

This specimen is from a case of broncho-pneumonia complicating a pseudo-membranous inflammation 
of the larynx in scarlatina. Exfoliated epithelium, leucocytes, and a little fibrin with the streptococci form 
the scanty exudate. 



micro-organisms. These pneumonias are not considered among the infec- 
tious diseases where they logically belong, partly because there are prac- 
tical advantages in grouping pulmonary lesions together and partly be- 
cause our knowledge of the relative frequency and significance of the 
bacterial excitants of the various types is still in many cases too incom- 
plete to permit the establishment of a distinctive and clearly defined 
form of infection. ^ 

' For a resume of the general results of the attempts to induce experimental pneu- 
monia in animals, consult Aufrecht in Nothnagel's "Specielle Pathologic u. Therapie," 
Bd. xiv., Th. 2, p. 36, bibliography, p. 221. 

For a stud}^ of bacteria in the lungs and their relationship to pneumonia, consult 
KUpsiein, Zeits. f. klin. Med., Bd. xxxiv., p. 191, 1898; also with special reference to 
children, see Dilrck, Deut. Arch. f. klin. Med., Bd. Iviii., p. 368, 1897. 

For a study of bacteria in the lungs of man and lower animals, see Beco, Arch, de 
Med. experimentale, etc., t. xi., p. 318, 1899, and t. xiii., p. 551, 1901. 

For a study of experimental cooling of the body which may induce changes in the 



460 



THE RESPIRATORY SYSTEM. 



Interstitial Pneumonia. 

This name is given to a chronic productive inflammation, which in- 
volves the connective-tissue framework of the lung and the walls of the 
air spaces, and results in the formation of new connective tissue and the 
obliteration of the air spaces (Fig. 252). 

Such an interstitial pneumonia may follow acute lobar pneumonia 
with the production of new intra- alveolar connective tissue, broncho- 
pneumonia, chronic pleurisy, chronic bronchitis, and atelectasis, or may 
be induced by the inhalation of the dust of coal, stone, or other inor- 
ganic substances. Diffuse interstitial pneumonia may occur in syphilis. 

The topography of the lesion varies considerably in the different con- 
ditions under which the new tissue growth occurs. If it follow acute 




4-^ 



J- 



X, 



>.(-ik 







"V^ 



•//i'?.; 



)mm 



Fig. 2")'^.— LIIROMC IMPRSTITIAL PNEUMONIA. 



lobar pneumonia, one lobe or the whole of one lung may be involved and 
covered with pleuritic adhesions. The lobe or the lung is small, smooth 
on section, and firm in texture. The air spaces and small bronchi may 
be largely obliterated by the new connective tissue. If it follow broncho- 
pneumonia, one or more lobes are studded with fibrous nodules, which 
correspond to the affected bronchi and the associated lung territory ; or 
a large part of a lobe is converted into dense fibrous tissue ; the pleura 
may be thickened ; there may be chronic bronchitis and bronchiectasia. 
If interstitial pneumonia be associated with thickening of the pleura, 
bands of connective tissue extend from the pleura into the lung, the 
bronchi are inflamed and often dilated. When associated with chronic 

blood, predisposing to infection with the pneumococciis, see BeinebotJi and KohUiardt, 
Deut. Arch. f. klin. Med., Bd. Ixv., p. 192, 1900. 

For a study of the effects of cooling in general as a predisponant to infection, see 
Kisskalt, Arch. f. Hygiene, Bd. xxxix., p. 142, 1900, bibliography. 

For a study of the portals of entrv in lung infection, with special reference to the 
pleura, see Grober, Deutsch. Arch. f. klin. Med^ Bd. Ixviii., p. 296, 1900, bibliography. 

Concerning circulatory changes in the lungs under various pathological conditions, 
see reference to Esser, p. 445. 



THE RESPIRATORY SYSTEM. 461 

bronchitis there are fibrous nodules around the bronchi, with more or 
less diffuse connective tissue. 

The changes in interstitial pneumonia may occur by a slow hyperpla- 
sia of the fibrous tissue or by the formation of granulation tissue which 












5 ^-'5 (Sii^ '^ 



Fig. 253.— Chronic Ixterstitial Pneumonia. Reversion of Epithelium in Isolated Air Vesicles. 

gradually becomes denser with contraction. Although this process is 
primary in the interstitial tissue, exudates are often present in the air 
spaces ; atelectasis may occur, while emphysema and bronchiectasia are 
common. 

Sometimes a noteworthy change occurs in the epithelium lining air 
vesicles which have been cut off from their neighbors by the new fibrous 
tissue. The epithelial cells increase in number, become thicker, and 
finally the small or distorted cavities may be lined with a complete in- 
vestment of cuboidal cells (Fig. 253). This reversion of the epithelium 
of the air vesicles to a less differentiated type occurs in many chronic 
processes in the lungs. 

Pigmentation of the Lung. — The inhalation of dust and smoke is so 
continuous among those who live much indoors that the lungs of nearly 





i 

'V 

Fig. 354.— Anthracotic Pigmentation of the Lung. 
Showing pigment beneath the thickened pleura and in the thickened septa of the emphysematous lung. 

all persons from the earliest years are more or less pigmented. The for- 
eign particles which get into the deeper recesses of the lungs are in part 
taken up by the epithelium of the air spaces, in part are carried by pha- 
gocytes or otherwise to the interstitial tissues of the lungs (Fig. 254). 
Here, either within cells or without, thej^ are deposited along and within 



462 THE EESPIEATOEY SYSTEM. 

the lymph-channels or in the lymph- nodules of the pleura and interstitial 
tissue, or they may be carried to the lymph-nodes at the root of the 
lungs. Earely, this inhaled dust passes the tracheal and bronchial 
lymph-nodes and may be deposited in the viscera, especially in the liver 
and spleen. 

Under ordinary conditions a considerable deposit of inhaled pigment 
particles in the lungs does not seem to be of great significance, though 
there is little doubt that it may predispose to more serious lesions. On 
the other hand, miners and others working or confined in smoky air, 
stone or metal workers, and the like are liable to excessive pigmentation 
and develop interstitial j)neumonia, especially marked at first along the 
interlobular septa and frequently associated with chronic bronchitis, 
emi^hysema, atelectasis, or bronchiectasia. This condition of the lung 
when due to the inhalation of coal dust is called anthracosis ; when due to 
dust of various minerals, clialicosis ; when due to iron dust, siderosis.^ 
The general process has been csilled jmeiimolioniosis. The color varies in 
these lungs with the character and amount of the deposited material, 
which is frequently quite unevenly distributed. The amount of foreign 
material in such lungs is sometimes large. ^ 



Tuberculous Pneumonia. 

General Considerations. — Tuberculous inflammation of the lungs is sim- 
ilar in nature to tuberculous inflammation in other parts of the body. 
But since the character of the response of a tissue to injury is largely 
dependent upon the form and capacities of its cells, it is not surprising 
that in such complex organs as the lungs, the lesions of tuberculosis 
should present many variations from the usual type elsewhere. The 
bronchial passages and the connecting air spaces, the numerous blood- 
and lymph-channels especially favor the distribution of the tubercle 
bacillus within these organs ; the open texture of the lungs permits, as in 
other forms of pneumonia, of great accumulation of exudate, while the 
delicacy and thinness of the air chambers favor extensive disintegration 
of the old or new-formed tissues or exudates when these have become 
necrotic under the influence of the poisons of the tubercle bacilli. ^ 

Thus the variety of cells and tissues involved and their peculiar rela- 
tionships to one another and to the invading organisms render the lesions 
of pulmonary tuberculosis more complex in morphology than are tuber- 
culous lesions in any other part of the body. 

The classification of these lesions is largely based upon topographic 
considerations and is not to be regarded as indicating fundamental differ- 
ences in the reaction of the tissues. 

^For a study of the condition of iron pigment in cells and tissues see Arnold, 
Virch. Arch., Bd. clxi., p. 284, 1900. 

'■^ For an analysis of the lungs of a case of extreme anthracosis see Hodenpyl, Trans 
New York Path. Soc, 1899-1900. 

^For further details concerning the lungs in inflammation see p. 449. 



Pathology — Delafield and Prudden. 



Plate IV. 




Miliary Tuberculosis (Acute) of the Lung. 

The miliary tubercles, small and irregular in shape, are distributed 
throughout the lung — more abundantly in the upper and middle thirds. 

The blood-vessels are injected with blue gelatin, so that in this 
photographic reproduction of the specimen the uninvolved portions of 
the lung are dark, while the tubercles — in which the blood-vessels are 
compressed or obliterated — are light. 



THE EESPIKATORY SYSTEM. 463 

Tubercle bacilli may enter the lungs either through the blood- and 
lymph -vessels, being brought from a focus of tuberculous inflammation 
in another i^art of the body ; or, as is more frecjuently the case, they are 
introduced through the air passages by the inhalation of floating dust 
particles, among which are living tubercle bacilli. 

The introduction of tubercle bacilli into the lungs may induce an 
exudative inflammation with the accumulation of fibrin, leucocytes, and 
exfoliated epithelium in the air spaces ; a productive inflammation with 
the growth of epithelial cells, or of round- celled tissue, or of a tissue 
comiDOsed of basement substance, large and small cells, and giant cells 
called tubercle tissue (see page 218) ; or there may be added necrosis of 
the new tissue and of portions of the lung. All of these phases of tuber- 
culous lesions may and usually do occur together. 

The character of the inflammation in each case seems to be governed 
by the type of cells especially involved, by the number, virulence, and 
proliferative capacity of bacilli which are introduced into the lungs, and 
the way in which these enter, as well as by the susceptibility of the indi- 
vidual. If a large number of virulent tubercle bacilli be inhaled or 
aspirated through the bronchi, or if the bacilli grow with great rapidity, 
both productive and exudative inflammations may be set up in a consid- 
erable portion of the lungs. If, on the other hand, but few bacilli enter 
and their proliferation or virulence be not extreme, or if these find their 
way in small numbers into the lungs through the blood-vessels or lym- 
phatics, then there may be small foci of productive inflammation with 
but little exudation. The tuberculous alterations in the lungs are usually 
accompanied or followed by a series of secondary processes which often 
complicate the condition of the patient as well as the morphological ap- 
pearances of the organs. The obliteration or destruction of the smaller 
blood-vessels of the lungs in the tuberculous areas contributes to the 
gray or whitish apiDcarance of the lesions, due largely to new-formed tis- 
sue or accumulated exudate. The formation of fibrous tissue in the 
attempts at repair of the damage wrought by the tubercle bacillus often 
dominates the structural picture. 

The traditional distinctions between acute and chronic forms of i^ul- 
monary tuberculosis are often morphologically not at all well defined and 
are of value chiefly for clinical purposes. 

It has been customary to set apart those forms of acute tu^berculosis 
of the lungs in which the lesions are in the form of small discrete so- 
called " miliary '^ foci, calling the condition Acute Miliary Tuberculosis. 
The other tuberculous lesions involving in varying degree the lungs and 
the bronchi with associated and often extensive exudative necrotic and 
reparative processes have been commonly jumbled together as Acute and 
Chronic Phthisis, many phases of which have been elaborately described 
as if they were the expression of independent processes. 

With our present knowledge of the nature and etiology of tuberculosis 
it seems better to let the word phthisis fall into disuse as speedily as 
possible and to consider under more exact and significant designations 



464 THE RESPIRATORY SYSTEM. 

such phases of pulmonary tuberculosis as the morphological characters 
of the lesions justify. We shall review the lesions of pulmonary tuber- 
culosis then under the following primary headings : 

1. Focal or miliary tuberculosis. 

2. Tuberculous broncho-pneumonia. 

3. Complex forms of nodular and diffuse tuberculosis lesions. 

4. The formation of cavities. 

5. Secondary lesions in pulmonary tuberculosis. 

6. Concurrent infection. 



Focal Tuberculosis. (Miliary Tuberculosis.) 

Acute Miliary Tuberculosis. — The rapid and widespread development 
of miliary tubercles in the lungs is often a part of general tuberculosis, 
although the lesion may be most extensive in the lungs. Both lungs are 
apt to be involved, but the distribution, number, size, and character of 
the miliary tubercles differ in different cases. The tubercles are found 
in the parenchyma of the lung, in the connective tissue forming the 






Fig. 355.— Miliary Tubercle of Lung. 



This tubercle has replaced several air vesicles whose walls are obliterated. In the centre is an area of 
coagulation necrosis, outside of this is a zone of organized tubercle tissue ; the surrounding air vesicles 
contain a cellular exudate. 

septa, along and in the walls of the bronchi and blood-vessels, and in the 
pulmonary pleura. They may be scattered singly through the lungs 
(Plate IV. ), or aggregated in groups (Plates VI. and VII. ). They may 
be separated by considerable interspaces, or so close together that the 



THE RESPIRATORY SYSTEM. 



465 



lung is rendered nearly solid. Some are so small and transparent that 
they can hardly be seen with the naked eye ; others are larger and more 
opaque and may have a lighter centre marking the area of necrosis. 

In many cases it is evident that the lungs are infected through the 
blood-vessels or the lymphatics, for the general tuberculous infection 
is secondary to a localized tuberculosis either in the lungs or in some 




Fig. 256.— a Miliary Tubercle of the Lung. 

Involving only two air vesicles, of which the walls are infiltrated and the cavities filled with tubercle 
tissue. The blood-vessels of the air vesicles are injected, except where these are obliterated by the tubercu- 
lous involvement of their walls. 



other part of the body. In a considerable proportion of cases of miliary 
tuberculosis of the lungs tuberculous lesions of the bronchial lymph- 
nodes or of the lung tissue at the apex of much longer standing indicate 
the probable immediate source of origin of the widely distributed tubercle 
bacilli. Very often in miliary tuberculosis of the lungs the tubercles in 
one part of the lungs are larger and appear to be older than those in 
other parts. Thus it is not infrequent to find the tubercles in the upper 
portion of the lungs more abundant, larger, and more fibrous than in the 
lower lobes (see Plate YII. ). It is in fact probable that in many cases 
of acute miliary tuberculosis of the lung, either associated or not with 
30 



466 



THE RESPIRATORY SYSTEM. 



older local tuberculous lesions from which the distribution of bacilli may 
have taken place, the generalization has not occurred at once but by 
successive fresh infections. ' 

Miliary tubercles in the lungs are in structure essentially similar to 
those formed elsewhere in the body, except that the filling of the air 
spaces with exudate makes the lesion somewhat more complex. 

The tubercles may be composed of small spheroidal cells or of larger 
polyhedral cells with more or less fibrous stroma, or of small and large 
cells and stroma. Giant cells may be present ; coagulation necrosis is 
usual (Fig. 114, page 220). Such forms of miliary tubercles may be and 
commonly are associated with the presence of an exudate in the adjacent 






,-># \^^:^^ 




Formed of a number of 



Fig. 357.— a Miliary Tubercle of the Lung. 

vesicles, some containing tubercle tissue, others pus and epithelium. The walls 
of the air vesicles are in part still preserved. 



or involved air vesicles (Fig. 255). This exudate may be largely made 
up of exfoliated epithelial cells which have x)rolif crated ; or with these 
there may be serum, leucocytes, and fibrin. The blood-vessels within 
the tubercles which replace the lung tissue are partially or wholly oblit- 
erated (Fig. 256). 

But the miliary foci of tuberculous inflammation in the lungs may 
consist wholly of inflammatory exudate which early becomes necrotic, 
often with necrosis of the walls of the involved airspaces (Fig. 115, page 
222). Such tubercles of the exudative type are apt to occur in children 
and usually contain large numbers of tubercle bacilli. They may occur 
in connection with various other phases of acute and chronic pulmonary 
tuberculosis. 

^ For references to the origin of miliary tuberculosis see Benda, Lubarsch and 
Ostertag's "Ergebnisse," Jahrg. v., p. 447. 



Pathology - Delafield and Prudden. 



Plate V. 




Tuberculous Broncho-Pneumonia. 

The walls of the smaller bronchi are involved, being thickened and 
caseous, while the ulceration of many of them has led to the formation 
of numerous small cavities. 

The blood-vessels are injected with blue gelatin, so that the less 
affected and the intact parts of the lungs are the darker. 



THE EESPIRATORY SYSTEM. 



467 



When miliary tubercles are situated in the parenchyma of the lung 
the walls of the air spaces may be visible in the new growth (Fig. 257) 
or they may be largely or wholly obliterated (Fig. 258). 



Fig. 258.— a Miliary Tubercle of the Lung. 

This tubercle is largely caseous, the walls of the involved air vesicles being merely indicated in ihedead 
mass by slightly stained streaks or bands. There is cellular exudate in the surrounding air vesicles. 



Chronic and " Healed " ^Vliliary Tubercles. — The small foci of tubercu- 
lous inflammation which are called miliary tubercles may, as we shall 
see later, extend and coalesce so that with more or less exudative pneu- 









,..r:y 



-;•■•: ^-' 






"^' ^^"^ ~ ^' ^ C':"^ ^ ■ -^ 



;..-% 
/ •''"*-'" 



My- 



Fig. 259.— a Fibrous Tubercle— "Healed Tubercle" of the Luxg. 

The centre is caseous, the fibrous tissue surrounding this is dense, the walls of the surrounding air spaces 
are thickened. A giant cell at the right is calcified. 



468 



THE RESPIRATORY SYSTEM. 



monia large areas of the lung may become consolidated, thus developing 
one of the forms of pulmonary tuberculosis called phthisis. 

On the other hand, small tuberculous foci in the lungs may with or 
without extensive necrosis become surrounded by or converted into masses 
of dense fibrous tissue. These fibrous tissue masses, which are often 
called ^^ healed tubercles" (Fig. 259), may contain necrotic material or 
they may be calcified at the centre. Tubercle bacilli may be absent from 
them or the bacilli may remain alive within them for a long time quies- 
cent, but, as Lartigau and others have shown, still virulent. When such 
circumscribed masses of more or less fibrous tubercle tissue are scattered 




Fig. 260.— Tuberculous Inflammation of the Lung with Cheesy Degeneration about the 
Bronchi in a Single Lobule of the Lung— Tuberculous Broncho-Pneumonia. 

through parts of the lungs, although they may be of considerable size, 
the process is sometimes called '^ chronic miliary tuberculosis,^' 

It should be remembered that the new fibrous tissue which forms in 
and about miliary tubercles, as well as other tuberculous lesions, is the 
result of a distinctly reparative process in which the already formed 
tubercle tissue or its products apparently act somewhat as foreign bodies 
may in inducing fibrous-tissue growth. 



Tuberculous Brois^cho-Pneumonia. 

In another most important phase of tuberculous inflammation of the 
lung there is an involvement of the walls of the smaller bronchi and the 
associated groups of air spaces. This may occur through inhalation of 



'athology — Delafield and Prudden. 



Plate VL 




Miliary Tubercles and Tuberculous Broncho-Pneumonia with 
Diffuse (Chronic) Tuberculous Lesions in the Apex. 

There is in the apex tuberculous consolidation with coagulation 
necrosis (caseation), new fibrous tissue, and a small cavity. The middle 
third of the lung contains many small single and clustered miliary tuber- 
cles and foci of tuberculous broncho-pneumonia. The lower third con- 
tains a few similar small tuberculous foci, also scattered and in clusters. 

The appearance of the lung leads to the conjecture that tubercle 
bacilli may have been gradually disseminated from the earlier lesion in 
the apex. The blood-vessels are injected with blue. 



THE RESPIRATORY SYSTEM. 



469 



bacilli or by their aspiration from an established tuberculous focus, for 
example, from a lesion at the apex, or, as is often the case in children, 
from tuberculous bronchial lymph-nodes ; or infection may take place 
through the blood- or lymph-vessels. In the early stages of tuberculous 
broncho -pneumonia the cut surface of the fresh lung may present small 
gray or yellowish-white areas of consolidation with necrosis clustered 
about the small or terminal bronchi (Plate Y. ). The process is at first 




Fig. 261.— Tuberculous Broncho-Pxeumoxia. 
A miliary tubercle In the walls of small bronchi. The blood-vessels are obliterated in the involved regions. 



largely exudative, involving a catarrhal and necrotic inflammation of the 
mucous membrane of the bronchus with more or less exudate— which also 
may soon become necrotic— in the associated groups of air spaces (Fig. 
260). Sometimes organized tubercle tissue may form in the walls of 
the bronchi with thickening of the walls and obliteration of the blood- 
vessels of the adjacent air spaces (Fig. 261). 

By the extension of the process from one and another affected bron- 
chus and the coalescence of these, large areas of the lungs may become 
involved. In this more advanced stage of broncho -pneumonia the larger 



470 



THE EESPIEATOEY SYSTEM. 




Fig. 262.— Tuberculous Broncho-Pnkumoxia. 

The walls of the bronchi are thickened and caseous and are surrounded by zones of exudative and 
caseous pneumonia. This cut shows a small region, more highly magnified, of a lesion similar to that 
shown in Plate V. 

and smaller consolidated areas may be dark red with firmer gray or yel- 
lowish-gray central portions, in which the blood-vessels are obliterated, 
or the whole area may be solid and in the fresh Inng grayish- white. This 




;^y't-C-^ 







Fig. 363.— Tuberculous Broncho-Pneumonia. 

The wall of this medium-sized bronchus is caseous, tubercle tissue is formed about it and is extending into 
the surrounding lung tissue. A cellular exudate is seen in the contiguous air vesicles. 



PaXhoXogy—Delafield and Prudden. 



Plate VII. 




Diffuse and Focal (Chronic) Pulmonary Tuberculosis^ 
" Chronic Phthisis." 

In the upper third of the lung there is tuberculous broncho-pneu- 
monia with commencing ulceration of small bronchi : nearly complete 
consolidation from the extension and coalescence of small tuberculous 
foci and diffuse formation of fibrous tissue. 

In the lower third of the lung are irregular, dense, sharply outlined 
tuberculous foci (chronic miliary tubercles). 

In the middle third there is tuberculous pneumonia of the exudative 
type, the incompletely consolidated areas having become, in part, caseous. 

The less involved portions of the lung in this, as in the other in- 
jected specimens, are the darker. 



THE RESPIRATORY SYSTEM. 



471 



new-formed tissue may undergo necrosis and ulceration so that with an 
advancing consolidation of the lung tissue about the bronchi numerous 
larger and smaller, rough, irregular cavities may be formed (Fig. 262). 
The walls of the larger bronchi also may become the seat of a tubercu- 
lous inflammation with more or less necrosis (Fig. 263). Ulceration 
of these necrotic bronchial walls may lead to the formation of ragged 
cavities (Plate IX. and Fig. 264). 

The secondary development of dense fibrous tissue in connection with 
tuberculous broncho -pneumonia is a marked feature of the persistent or 
chronic forms. Tuberculous broncho -pneumonia is one of the most im- 




FiG. 264.— Tuberculous Broncho-Pneumonia. 

Showing the formation of cavities in the lung in acute phthisis. To the right are small, in the centre 
large tuberculous bronchiectatic cavities. At the left are areas of tuberculous consolidation with caseation 
in their central portions. 

portant of that complex of pulmonary lesions called phthisis, and is com- 
monly associated with other forms of tuberculous involvement of the 
organ — miliary tubercles, larger areas of consolidation, etc. 



Complex Forms of j^odular and Diffuse Tuberculous Lesions. 

(FJithisis. ) 

With or without the various well-defined forms of tuberculous bron- 
cho-pneumonia and miliary tubercles above described, there may be 
more or less circumscribed small or large areas of productive and exuda- 
tive tuberculous inflammation of the lung with necrosis, both of the lung 
tissue, the new -formed tissue, and the exudate (Plate XII. ). These may 



472 



THE RESPIRATORY SYSTEM. 



develop as the result of fresh infections of the lung through the lym- 
phatics or otherwise. These areas or nodules may coalesce so that whole 
lobes or j)arts of lobes of the lungs may become consolidated (Plates YII. 
and YIII. ) . Microscopically, these consolidated areas may be composed 
of tubercle tissue more or less necrotic, with partial or total obliteration 
of the walls of the air spaces. On the other hand, when the process has 
been exudative as well as productive in character, one may see in the solid 





r 




X.. 



v^ 




Fig. 265.— An Air Vesicle Filled with Fatty Epithelium, in Chronic Pulmonary Tuberculosis. 
The wall of the air vesicle Is diagrammatic. 



areas the outlines of the air vesicles and larger spaces; but these, 
together with the enclosed exudate, may be necrotic and granular with 
few stained nuclei and fragments of chromatin. Much of the exudate 
which fills the air vesicles either within or about these more densely con- 
solidated areas may not be caseous or necrotic, but may consist of well- 
preserved or fatty epithelial cells (Fig. 265), or of these with varying 
quantities of leucocytes and fibrin. 

Aside from these complex forms of nodular and diffuse tuberculous 
lesions one may recognize a Diffuse Exudative Tuberculous Inflammation of 



ithology — Delafield and Prudaen. 



Plate VIII. 




Diffuse (Chronic) Pulmonary Tuberculosis- 
Phthisis." 



Chronic 



In the upper haK of the lung there are scattered miUary tubercles 
and irregular areas of consolidation, with a diffuse formation of fibrous 
tissue; the pleura is thickened. A large portion of the lower lobe is 
densely consolidated from tubercle tissue and exudate with coagulation 
necrosis of the involved regions. These regions are light in color, 
dense, hard, and bloodless. Such dead caseous areas may persist for 
some time, or may soften and disintegrate, giving rise to cavities. 



THE EESPIKATORY SYSTEM. 



473 



the Lungs of Acute and of Chronic Type, — Cheesy Pneumonia; Pneumonic 
Phthisis. 

1. Acute Type. — Sometimes large areas or whole lobes or the whole 
lung may be the seat of an exudative i)rocess by which the affected region 







\ 







Fig. 266.— acutk Pulmoxary Tuberculosis— exudative Type (Acute Phthisis— Cheesy Pneumo- 
mia): with extexsite dlsixtegratiox axd formation op cavities. 

The pleura is much thickened. 



becomes solidified, the exudate consisting of epithelium with more or less 
fibrin and pus. This exudate, together with the lung tissue, soon under- 
goes necrosis, so that the solidified lung becomes dense, mottled, and 
gray in color. Extensive disintegration (Fig. 266) of the consolidated 



474 THE RESPIRATORY SYSTEM. 

and necrotic portions of the Inng may take place with the formation of 
large ragged cavities (see Plate X.). In many cases enormous numbers 
of tubercle bacilli are present in the exudate of the involved region in 
this type of exudative and necrotic pulmonary tuberculosis. 

2. Chronic Type. — There may be a more gradual development of 
the exudate, involving larger or smaller areas, often with tuberculous 
thickening and necrosis of the walls of the air spaces. With this as with 
other forms of pulmonary tuberculosis there may be associated a growth 
of simple fibrous tissue with the formation of cavities. 

Not infrequently the exudate in such forms of diffuse tuberculous in- 
flammation of the lung is less cellular and more serous or sero -fibrinous 
in character when the appearance of the consolidated region is trans- 
lucent and gelatinous. 

Obliteration of the larger blood-vessels by thrombosis or inflamma- 
tion of the wall often plays an important part in most forms of tubercu- 
lous lesions of the lungs. When large trunks are involved, large lung 
areas, supplied by the occluded vessels, particularly those in which exu- 
date is present, may become necrotic en masse, then often appearing on 
section smooth, shining, grayish-white in color, and bloodless. 



The Formation^ of Cavities in Pulmonary Tuberculosis. 

We have seen that in tuberculous broncho -pneumonia ragged cavities 
may form by a progressive necrosis and disintegration of the thickened 
walls of the affected bronchi and the adjacent lung tissue (Plate IX. 
and Fig. 264). Similar destructive alterations may occur in the areas of 
tuberculous and necrotic tissue which involve larger and smaller portions 
of whole lobes (Plate XL). This is most often rapid and extensive- in 
solidified and necrotic areas of the exudative type (Plate X. and Fig. 
266). These ragged cavities may communicate with one another as well 
as with the bronchi. 

While at first without distinct limiting walls, if the necrotic process 
be not too active and extensive, new fibrous tissue may gradually form 
about tuberculous cavities (Plate XII. and Fig. 267); and these may 
become lined with granulation tissue or a layer of new-formed tubercle 
tissue. Here an enormous proliferation of tubercle bacilli may occur for 
long periods. These may be cast out in the sputum or aspirated into other 
parts of the lungs. The old blood-vessels of the involved portion of the 
lung may lie upon the walls or stretch across these cavities, sometimes with 
obliterated lumina, sometimes still permeable, and from these haemorrhages 
may occur. There may be continuous and prolonged suppuration of the 
walls of the cavities and putrefactive processes may be incited by the 
advent through the air passages of various forms of bacteria. The walls 
of cavities may become fibrous with an arrest of the tuberculous process, 
and they may become shut off from bronchial communication. 



F2X\\o\ogY—Delafield and Prudden. 



Plate IX. 




Tuberculous Bronchiectatic Cavities in Pulmonary 
Tuberculosis. 

The advancing tuberculous involvement of the walls of the larger 
bronchi in the upper lobe is associated with ulceration, so that the bron- 
chiectatic cavities gradually become larger. In the upper portion of the 
upper lobe there is diffuse consoHdation with caseation : the lower 
portion of the lobe shows miliary tubercles and partial consolidation of 
the lung about them by exudate. 

The lower lobe is free save for a few scattered tubercles. The 
blood-vessels are injected with blue so that the uninvolved portions of 
the lung are dark. 



THE EESPIitATORY SYSTEM. 



475 



Secondary Lesions in Pulmonary Tuberculosis. 



A variety of secondary processes may be associated with the various 
phases of pulmonary tuberculosis which we have briefly reviewed. The 
blood-vessels in affected regions may be intact, or, as we have seen, their 
walls may be involved in the productive and necrotic processes, with 
thrombosis or obliteration of 
the lumen ; or more or less ex- 
tensive haemorrhages may oc- 
cur. If the consolidation be 
not complete, lung tissue, often 
in a condition of atelectasis or 
emphysema and with more or 
less cellular or granular exu- 
date, may remain between the 
tuberculous areas. Miliary 
tubercles may be scattered 
among the larger consolidated 
masses or in parts of the lung 
otherwise free. 

In chronic forms of pul- 
monary tuberculosis the an- 
thTdbGOiio, pigment is often con- 
spicuous, particularly in the 
cheesy and fibrous areas, stand- 
ing out in masses and streaks 
in contrast to the new or dead 
tissue. Furthermore, there 
may be associated with the 
lung lesions acute exudative or 
chronic fibrous pleuritis with 
adhesions ; o r tuberculous 
pleuritis of varying extent; 
empyema and pneumothorax. 
There is nearly always more or 
less chronic catarrhal bronchitis 
or broncho-pneumonia and fre- 
quently bronchiectasia. 

Tuberculous inflammation 
in the bronchial lymph-nodes 
frequently accompanies and often precedes the development of pulmo- 
nary tuberculosis. In children the tuberculous lymph-nodes often extend 
far into the lung and may on softening give rise to cavities at a consider- 
able distance from the hilus of the lung. 

Tuberculosis in other parts of the body is common in connection with 
pulmonary tuberculosis. 




Fig. 267.— Chronic Pulmonary Tuberculosis 
(Chronic Phthisis), with Cayities. 

There is much dense flbrous tissue in the upper lobe 
surrounding and between the cavities as well as in the 
upper portion of the lower lobe. 



476 THE RESPIRATORY SYSTEM. 

In all these various processes new -formed fibrous tissue, not tubercu- 
lous in character, may develop, variously distorting the lungs and 
sometimes enclosing the tuberculous areas. There is much reason for 
the belief that the characteristic so-called tubercle -tissue formation in all 
phases of tuberculosis is a response of the living cells to injury, which as 
in other phases of inflammation is fundamentally conservative (see page 
126). But whether this be so or not, it is certain that it is through the 
development of fibrous tissue, which is so important a feature in persis- 
tent phases of pulmonary tuberculosis, that the delimitation or replace- 
ment of tuberculous foci, the encapsulation of tuberculous cavities, etc. , 
occurs. While, therefore, fibrous-tissue formation in the lung is fre- 
quently associated with the necrotic and other destructive tuberculous 
lesions, and is often a v^ery conspicuous factor, it should be remembered 
that the healing which takes place in the majority of cases in man after 
moderate infection is achieved through its agency. 

It is especially upon the presence or absence of fibrous tissue in the 
lesions that the distinction between acute and chronic phthisis is based. 

It will be seen from this brief outline of various prominent phases 
of pulmonary tuberculosis that the gross appearances of the lungs are 
most diverse, although the processes by which these changes are induced 
are few and comparatively simple. While no two lungs are quite simi- 
lar in the complex phases of the lesion, systematic gross and micro- 
scopical examinations soon enable the student to recognize the type of 
lesion under great complexity of detail. 



The Distribution" of the Lesions in Pulmonary Tuberculosis. 

Aside from general miliary tuberculosis in which the tubercles are 
widely distributed throughout one or both lungs, the most common seat 
and starting-point of tuberculous lesions in adults is the apical region or 
the depth of the lung, particularly the right, somewhat below the apex. 
In children, the tuberculous process more frequently commences in the 
bronchial lymph -nodes (Plates III. and XI.). 

From the apex the tuberculous process may extend downward, and 
with various forms of lesions involve more or less of the lungs. It is 
common to find at autopsies older fibrous lesions about the apices while 
marks of more active processes are to be seen below (Plate XII.). In a 
considerable percentage of bodies examined at autopsies, small and often 
healed tuberculous foci are found at the apex or in the bronchial lymph- 
nodes without evidence of extension of the process. 

Concurrent Infection in Pulmonary Tuberculosis. 

While it has been definitely established that tubercle bacilli are the 
excitants of both the productive and exudative forms of tuberculous 
inflammation, these bacilli are not infrequently associated in pulmonary 
tuberculosis with other organisms, especially with the Streptococcus and 



Pathology — Delafield and Prudden. 



Plate X. 




Pulmonary Tuberculosis — Exudative Type — with Large Cavities. 

The entire lung is solid from new-formed tubercle tissue and exudate which are both 
largely in a condition of coagulation necrosis. 

The thickened trunks of the larger pulmonary vessels are exposed in the depths of 
the ragged communicating cavities. 

This lung was hardened in alcohol without injection of the blood-vessels. 



THE EESPIEATOEY SYSTEM. 



477 



Staphylococcus pyogenes, with Micrococcus lanceolatus, and the influenza 
bacillus. 

There is reason to believe that in many cases at least the concurrent 
infection of tuberculous lungs with the Streptococcus pyogenes may be an 
important factor in the formation of cavities in areas of consolidation 
already established. ' The pyogenic cocci apparently play an important 
part in the bronchitis which so often accompanies acute and chronic 
phthisis. 

Artificial Pulmonary Tuberculosis in Animals. 

Much light may be gained upon the successive steps in the development of the 
lesions of pulmonary tuberculosis as well as upon the rapidity with which in a suscept- 




FiG. 268.— Experimental Tuberculous In- 
flammation (Miliary) in the Lung of a 
Rabbit. 

The rabbit's lung shows miliary foci of tubercu- 
lous inflammation, twenty-two days after the in- 
jection through the trachea of a small quantity of 
broth culture of the tubercle bacillus. 



Fig. 269.— Experimental Tuberculous Inflam- 
mation in the Lung of a Rabbit. 

Large areas of solidification in the lung twenty- 
eight days after the injection through the trachea of 
a considerable quantity of a pure culture of the tu- 
bercle bacillus. The lesions resemble those of 
acute phthisis in man. 



ible animal the lesion may develop, by the study of the tuberculosis artificially induced 
in rabbits with pure cultures. 

' For bibliography of concurrent infection in tuberculosis see Lartigau's article on the 
bacteriology, pathology, and etiology of tuberculosis, " Twentieth Century Practice of 
Medicine," vol. xx. ; also, for special bibliography of concurrent infection in pulmonarj'- 
tuberculosis, see Marfan, Bouchard and Brissaud's "Traite de Medecine," t. vii., p. 234. 



478 



THE RESPIRATORY SYSTEM. 



By the injection of tubercle bacilli alone and associated with streptococci into the 
lungs of rabbits through the trachea, it has been possible to reproduce very closely the 
lesions of pulmonary tuberculosis in man.^ 

If a small quantity of a pure culture of the tubercle bacillus in very minute flocculi 
be mixed with a considerable quantity of salt solution and introduced into the lungs 
of rabbits through the trachea a number of small areas of consolidation are produced 

which have the gross appearance of 
miliary tubercles (Fig. 268). These 
small areas of consolidation are com- 
posed of epithelial cells and leuco- 
cytes. After the development of 
these cell masses, which may occur 
within a few hours, they may remain 
with little apparent change, or be- 
come more or less infiltrated with leu- 
cocytes, or become cheesy, or be sur- 
rounded by a dense zone of small 
spheroidal cells ; or small foci of new 
tissue with more or less exudate, and 
necrosis may form. 

When larger quantities of the 
tubercle bacillus are introduced into 
the lungs through the trachea large 
areas of consolidation are formed 
(Fig. 269), which may involve whole 
lobes or whole lungs. 

Microscopically, these consoli- 
dated areas are practically identical 
with those which are found in man 
in various forms of tuberculous bron- 
cho-pneumonia. A later fibrous-tis- 
sue development may occur, and 
blood-vessels may be obliterated. 

In the presence of the tubercle 
bacillus alone the consolidated and 
caseous areas rarely soften and break 
down so as to form cavities. If, how- 
ever, after the tuberculous lesion of 
the lung has been induced and allowed 
to continue for a number of days, a 
culture of Streptococcus pyogenes be 
introduced into the trachea of the rab- 
bit, within twenty-four hours the 
caseous areas often begin to soften. 
The softening may begin at the cen- 
tre, or may surround a central por- 
tion of the necrotic mass. The softening is soon followed by absorption, and so cavi- 
ties are formed of varying sizes and shapes (Fig. 270). 

It will thus be seen that in the rabbit a concurrent infection with the tubercle bacil- 
lus and the streptococcus has an important bearing upon the breaking down of lung 
tissue which leads to the formation of cavities. While it would not be wise to assume 
from these experiments on the rabbit that a similar condition is always present when 
cavities form in man, we have seen that in fact a similar concurrent infection in man in 
acute phthisis actually does often exist. 

1 Prudden, New York Medical Journal, July 7th, 1894, 




Fig. 370.— Experimental Tuberculous Inflamma- 
tion IN the Lung op a Rabbit, with the formation 
OF Cavities. 

The lung was injected with a considerable quantity of 
tubercle-bacillus culture through the trachea, followed 
after twenty-eight days by the injection of the broth cul- 
ture of the Streptococcus pyogenes. Animal killed seven 
days after the streptococcus injection. The specimen 
shows large areas of consolidation with cavities. The 
lesions resemble those of acute phthisis with cavities in 
man. 



Pathology — Delafield and Prudden. 



Plate XI. 




Pulmonary Tuberculosis (Chronic), with Large Cavities. 

The ragged communicating cavities involve a large part of the lung and are bronchiec- 
tatic in origin. The bronchial lymph-nodes are enlarged, tuberculous, and caseous. The 
pleura and interlobar septum are thickened by the formation of dense fibrous tissue. 



THE KESPIRATOItY SYSTEM. 



479 



Syphilitic Pneumonia. 

Persons suffering from inherited or acquired syphilis sometimes 
develop inflammations of the lungs which seem to be due to the syphi- 
litic infection. The lungs may then be affected in several different ways. 




FIG. 371.— ENDOTHELIOMA OF THE LUNG. 

The growth is in the subpleural lymph-vessels, which seen from the pleural surface in the fresh lung 
formed a white raised network over a considerable portion of one lung. The lymph-vessels in the cut are 
seen in transverse section. 

There may be well-defined large or small gummata with or without 
interstitial and more or less exudative pneumonia. There may be a for- 
mation of new fibrous tissue in the walls and lung tissue about the bron- 
chi, often with ulceration of the mucous membrane and distortion of 
these structures. There may be, particularly in the new-born, lobular 
or lobar hepatization, the affected region appearing reddish or gray or 
white. This is due to a growth of new cellular tissue in the walls of the 




Fig. 273.— Primary Adenoma of the Lung. 



air spaces and to an exudate largely of epithelial cells in the air spaces. 
Infarctions of the lung from obliterating endarteritis may be present. It 



480 



THE RESPIRATORY SYSTEM. 



is often difficult to determine in many cases of interstitial inflammation 
of the lungs whether the lesion be syphilitic or not. ^ 



TUMORS. 



Fibroma and osteoma are rare. Enchondroma may occur as a primary 
tumor originating in the cartilages of the bronchi. Sarcoma is not 

common and is usually sec- 
ondary. '< Lymphoma " may 
develop in the lungs in leu- 
kaemia and pseudo -leukaemia. 
Endothelioma is of occasional 
occurrence in the lung and 
following the subpleural 
lymph- vessels may form a 
reticular raised white net- 
work on the surface of the 
lung (Fig. 271). Adenoma 
as a primary tumor is rare 
(Fig. 272). Primary carci- 
noma of the lung, originat- 
ing in the bronchi, is of 
occasional occurrence. " It 
may be associated with exu- 
dative pneumonia and in- 
volve large portions of the 
lungs as well as the pleura. 
Secondary carcinoma of the 
lung is not infrequent. The 
malignant growths in the 
lung may occur as circum- 
scribed nodular masses, dis- 
placing the lung tissue (Fig. 
273), or they may infiltrate 
the lung, often following the 
bronchi and larger blood- 
vessels. The cells of such 
tumors often grow into and 
fill up the air spaces of the 
lung, over large areas, without immediate involvement of their walls. ^ 
Dermoid cysts have been found in the lung. 

^ For i-ecent bibliography of pulmonary syphilis consult Flockemann, Centralhl. f. 
Path, und path. Anat., Bd. x., p. 449, 1899. 

2 See Passler, Virch. Arch., Bd. cxlv., p. 191, 1896, bibliography. 

3 For a consideration of the diagnosis of malignant tumors of the lung consult Adler, 
New York Medical Journal, February 8th and 15th, 1896, bibliography. 




Fig. 273.— Secondaky Carcinoma of the Lung. 

The primary tumor involved the gall ducts, liver, and 
pancreas. The metastatic tumors in the lung were in 
part white, in part dark red from interstitial haemor- 
rhage. 



Pathology — Delafield and Prudden 



Plate XII 




Chronic Pulmonary Tuberculosis with a Fibrous-Walled 
Cavity at the Apex. 

The fibrous wall of the cavity is dense and is continuous with the 
greatly thickened pleura and with the diffuse new-formed connective 
tissue throughout the upper lobe. The upper lobe is greatly reduced in 
size by the cicatricial contraction of the fibrous tissue. The lower lobe 
shows two areas of tuberculous consolidation ; both are caseous in the 
central portions ; the upper shows commencing tuberculous bronchiec- 
tasia. The upper part of the fibrous wall of the cavity, firmly adherent 
to the thoracic wall, has been cut awav. 



y 



THE DIGESTIYE SYSTEM. 



497 



/' 



Si *&©< 



,#: 



'■:-t'% 



'^^^■-^ 



Fig. 280.— Chronic Gastritis. 

Showing new - formed fibrous tissue between 
the gastric tubules. 



pyaemia, typhoid fever, the exanthemata, and other infectious, and may 
follow the ingestion of irritant poisons. The excitants are thus of the 
most varied kinds, as is the case in pseudo-membranous inflammation 

elsewhere in the body. The false 
membrane may be in small patches or 
line a considerable portion of the 
stomach. 

Exudative Gastritis (Suppurative or 
Phlegmonous Gastritis). — This process 
is characterized by the formation of 
puruleut and other exudate in the 
connective tissue of the mucosa and 
submucosa. The exudate may be 
diffuse or localized in the form of ab- 
scess. As an independent affection 
it is rare. It is more frequent in 
connection with puerperal fever and 
other infectious diseases ; it has been 
ascribed to injury. 

The accumulation of exudate may 
be slight, the interglandular and sub- 
mucous tissue being oedematous with few idus cells. The mucous mem- 
brane may under these conditions remain intact or show slight ca- 
tarrhal lesions. When this relatively slight accumulation of exudate 
occurs in the pyloric region it may apparently occasion temporary 
stenosis. On the other hand, a considerpible or large amount of exu- 
date may form, and the process 
may involve diffusely a large 
part of the wall of the stomach ; 
or the process may be circum- 
scribed and abscesses may form. 
The sux)purative process may ex- 
tend to the mucous membrane, or 
to the serosa, and thus perfora- 
tions may occur and the incite- 
ment of peritonitis. Little is 
known of the direct excitants of 
phlegmonous gastritis.' Strepto- 
coccus pyogenes has been found 
in the exudate." 

Toxic Gastritis. — The mineral 
acids, the caustic alkalies, arsenic, corrosive sublimate, and the metallic 



# 



'4 



5^ * 



, y^ '-^ 



Fig. 281.— Chronic Gastritis. 

Showing atrophy of the mucous membrane witli 

much new-formed fibrous tissue. 



^ Reference to the bibliography of micro-organism of the normal stomach may be 
found in an article by Weiss on "Bacteria in the Stomach of the Cat," .Jonr. of Applied 
Microscopy, vol. iii.,^p. 827, 1900; also Coyon, "Flore microbienne de restomac," These 
de Paris, 1900, bibliography. For bibliography of phlegmonous gastritis see Leitli, 
Edinburgh Hospital Reports, vol. iv., p. 51, 1896. 

•See Kinnicuit, Trans. Assn. Am. Phys., vol. xv., p. 127, bibliography. 
32 



498 THE DIGESTIVE SYSTEM. 

salts, phosphorus, camphor, and other irritating materials, induce differ- 
ent lesions of the stomach, according to their quantity, their strength, 
and the length of time which has elapsed before death. 

In large quantities they destroy and convert into a soft, blackened 
mass both the mucous membrane and the other coats, so that jDcrf oration 
may take place. In smaller quantities they produce black or white 
sloughs of the mucous membrane, surrounded by a zone of intense con- 
gestion. If death does not soon ensue, the ulcerative and cicatricial 
13rocesses which follow such sloughs may contract and deform the stom- 
ach in various ways. 

If the poisons are of less strength they may induce a diffuse conges- 
tion of the mucous membrane, with catarrhal or croupous exudation on 
its surface and serous infiltration of the submucous coat (see chapter on 
Poisons). 

Tuberculous Gastritis of the stomach is rare and is usually secondary 
to tuberculous lesions elsewhere. There may be miliary tubercles or 
small or large, single or multiple ulcers involving especially the mucosa 
and submucosa. ' 

Syphilitic Inflammation of the stomach with ulceration has been occa- 
sionally observed.' 

ULCERS OF THE STOMACH. 

Chronic Perforating Ulcer. — This form of ulcer is often seen ; according 
to Brinton, in five per cent of persons dying from all causes. It occurs 
in females nearly twice as frequently as in males. As regards the age, 
Brinton concludes that the liability of an individual to become the sub- 
ject of gastric ulcer gradually rises, from what is nearly a zero at the 
age of ten to a high rate, which it maintains through the period of mid- 
dle life ; at the end of which period it again ascends, to reach its maxi- 
mum at the extreme age of ninety. 

The analysis of 793 hospital cases by Welch ^ shows that the ulcers 
were on the lesser curvature in 288, in the posterior wall in 235, at the 
pylorus in 95, on the anterior wall in 69, at the cardia in 50, at the fun- 
dus in 29, on the greater curvature in 27. 

As regards the number of ulcers, two or more are present in about 
twenty-one per cent ; there may be two, three, four, or even five ulcers. 
In cases of multiple ulcers these are often developed successively. 

In size the ulcers vary from one-quarter of an inch to five or six 
inches. They are usually of circular shape, sometimes oval ; sometimes 
two or more are fused together. 

The ulceration is largest in the mucous membrane (Fig. 282). It 
may remain confined to this, or extend outward and involve the connec- 

' Consult for bibliography of tuberculosis of stomach Blumer, Albany Medical An- 
nals, March, 1898. 

-Consult for bibliography Flexner, American .Journal of Medical Sciences, vol. 
cxvi., p. 424, 1898. 

^ Welch, Pepper's "System of Practical Medicine," vol. ii., p. 504, 1885. Many im- 
portant data are to be found in this excellent article. 



THE DIGESTIVE SYSTEM. 499 

tive tissue, muscular aud peritoneal coats, its diameter becoming smaller 
as it advances. The ulcer looks like a clean hole punched out of the wall 
of the stomach. Its floor may show no active inflammatory changes. 
Its edges may be in the same condition, or they may be thickened by the 
growth of connective tissue and cells. The rest of the mucous mem- 
brane of the stomach is apt to be in a condition of chronic catarrhal 
inflammation. 

The ulcer may i^erf orate directly through the wall of the stomach, 
and the contents of the latter are discharged into the iDcritoneal cavity ; 
or adhesions are formed between the wall of the stomach and the neigh- 
boring viscera, so that the bottom of the ulcer is closed ; or if the liver, 
the intestines, or the abdominal wall become adherent, these may be 
invaded by the ulcerative process, and cavities or fistulse are formed 
communicating with the stomach ; or, if the adhesions are incomplete, a 
local peritonitis and collections of pus may be developed. Perforation 



Fig. 283.— Chronic Ulcer of the Stomach. 
Showing a section through the stomach wall at the central part of the round ulcer. 

may take place into the colon or duodenum, or into the pericardium or 
pleura. 

During the progress of the ulcer there may be repeated small haemor- 
rhages from the erosion of small blood-vessels, or large h£emorrhages 
from the erosion of larger arteries. 

In many cases these ulcers cicatrize, and such a cicatrization may 
produce various deformities of the stomach. I 

The origin of such ulcers is often obscure. It seems probable that the j 
nutrition of a circumscribed ]Dart of the wall of the stomach is interfered ! 
with, and that this portion is then destroyed by the action of the gastric 
juice. But we are in most cases still ignorant of the way in which the i 
obliteration of the arteries is effected. It has, indeed, been demonstrated I 
in animals that an artificial embolism of the branches of the gastric ar- 
teries may lead to ulcers of the stomach ; and in the human stomach we 
occasionally find cases of embolism of the branches of the gastric artery 
and ulcers. But the clinical history of most cases of ulcer of the stom- 
ach does not correspond with such a mode of origin. A chronic oblit- 
erating endarteritis would seem to be a more probable cause. The pos- 
sibility of a bacterial origin in some cases should not be overlooked. 



500 THE DIGESTIVE SYSTEM. 

Follicular Ulcers, similar to those in the small intestine, are of occa- 
sional occurrence in the stomach. They are formed by the degenerative 
changes and necrosis in the solitary lymph -nodules of the stomach. 

For Tuberculous Ulcers, see above. 

Hsemorrhagic Erosions occur as rounded spots or narrow streaks, 
formed by a loss of substance of the mucous membrane. The mucous 
membrane at these points may be congested, soft, and covered by small 
blood clots. The destruction of the mucous membrane is usually super- 
ficial, but may involve its entire thickness. The internal surface of the 
stomach may be studded with these erosions. They give rise to repeated 
hgemorrhages, and are accompanied by catarrhal inflammation of the 
rest of the mucous membrane. 

They occur at all periods of life, even in infants. Their usual seat is 
the pyloric portion of the stomach. They may occur independently of 
other obvious lesions, but are most frequent in connection with chronic 
congestion of the mucosa, chronic gastritis, in infectious diseases, and 
intoxications. 

DILATATION. 

Yery considerable degrees of dilatation of the stomach are found at 
autopsies, without stenosis of the pylorus or other mechanical cause to 
account for them. It is usually difficult to determine how long these 
dilatations have existed and their influence in the illness or death. 

Acute dilatation of the stomach, with vomitiiDg of very large quantities 
of thin fluid, has been observed in a few cases, the dilatation being 
developed suddenly and without discoverable cause. 

Of the mechanical factors which lead to dilatation of the stomach 
a stenosis of the pylorus is the most common. Such a stenosis may be 
effected by a tumor, by chronic inflammation and thickening, and by 
the cicatrization of ulcers. Less frequently obstructions of the small and 
large intestines act in the same way. 

Some forms of chronic gastritis are attended with dilatation of the 
stomach without stenosis. 

In rare cases circumscribed, sacculated dilatations are produced by 
the presence of foreign bodies — portion of wood, metal, etc. 



TUMORS. 

Papillomata. — It has already been mentioned that in some cases of 
chronic gastritis there are small, polypoid hypertrophies of the mucous 
membrane. Besides these we flnd polypoid tumors which may reach a 
considerable size. They are composed of a connective-tissue stroma 
arranged in tufts covered with cylindrical epithelium. In some cases 
there are also tubules lined with cylindrical epithelium, so that the 
tumor has partly the structure of an adenoma. Fibromata of small size 
are sometimes found in the connective -tissue coat (Fig. 283). Lipomata 



THE DIGESTIVE SYSTEM. 501 

are formed in the submucous connective tissue in the shai^e of rounded 
or polypoid tumors. They usually project inward, but sometimes out- 
ward beneath the peritoneum. They may also a^Dpear in the form of 
numerous yellow nodules beneath the mucous membrane. 

Myomata occur in the form of rounded tumors which originate in the 
muscular coat, but may gradually separate themselves from it and project 
inward or outward. The submucous myomata are at first small tumors 
lying loosely attached in the submucous tissue. As they grow larger 
they push the mucous membrane inward and take the shape of polypoid 
tumors. Lymphomata in the wall of the stomach are seen in some cases 
of leukaemia. 

Sarcomata of the stomach are rare. In some of the tumors of the wall 
of the stomach, which are ordinarily called cancerous, the structure is not 




Fig. 283.— Fibroma in the Wall of the Stomach of a Chh.d. . 
There were several of these small tumors In the wall of the stomach. 

well defined, and it is possible that some of them are sarcomata. Sarco- 
mata of the stomach may be round-celled or spindle -celled and mixed 
forms occur — myxosarcoma, angiosarcoma, etc. ^ 

Adenoma. — It has been already mentioned that in some of the x>apil- 
lary tumors of the mucous membrane there is a considerable growth of 
tubules lined with cylindrical epithelium. Besides these we find in the 
submucous coat circumscribed tumors comxDosed of tubules irregular in 
form and lined with one or more layers of cylindrical epithelium, like 
those of the gastric mucous membrane. (See Adeno- carcinoma below. ) 

Carcinoma of the stomach is usually primary but is occasionally sec- 
ondary to cancer elsewhere. It is of relatively common occurrence, the 
stomach in AYelch's analysis of over 30,000 cases being next to the uterus 
the organ most frequently affected. 

^ See Bock, Trans. Assn. Am. Phys., vol. xv., p. 165, bibliography; also Fenwick, 
Lancet, 1901, vol. i., p. 463, bibliography. 



502 THE DIGESTIVE SYSTEM. 

The situation in AYelch's summary of 1,300 cases' was: in the pyloric 
region, 791; lesser curvature, 118; cardia, 101; posterior wall, 68; 
involving a greater part of the stomach, 61; greater curvature, 34; 
anterior wall, 30 ; fundus, 19 ; multiple tumors in 45 cases. Carcinoma 
of the stomach is rare in childhood. ' 

Carcinomata of the stomach occur in various forms. There may be 
larger or smaller, flat or rounded or lobulated growths projecting from 




■> Fig. 284.— Hair Balls from Human Stomach. 

This specimen consists largely of hairs, cotton and woollen threads, straws, etc. 

the inner surface of the stomach. The mucous membrane over them 
may be intact or with a portion of the tumor may ulcerate. The destruc- 
tive process may advance so that some of the ragged or smooth-edged 
ulcers may reach a large size. The wall of the stomach may be involved ; 
peritoneal adhesions may form, or perforation may occur. On the other 
hand, the carcinoma may grow in the form of a diffuse infiltration of the 
wall of the stomach. Such tumors are less liable to ulcerate. They 
may be overlooked or mistaken for a chronic inflammatory lesion. 

Metastatic tumors in the liver, the lymph-nodes, and the peritoneum 
are common, but such metastases may occur in any part of the body. 

The most common type of carcinoma of the stomach is the medullary, 
or so-called adeno- carcinoma, in which often to a considerable extent the 
glandular type is maintained in many parts of the growth (Fig. 173, 
page 307). The cylindrical or polyhedral epithelial cells line variously 
shaped alveoli, which frequently maintain well-marked lumina. Cystic 
distention of these may occur. 

Fibrous carcinoma, scirrhiis, is the next most frequent type, and such 
are often the infiltrating forms (Fig. 189, page 318). 

^ Welch, Pepper's "System of Practical Medicine," vol. ii., p. 561, 1885. 
2 See Osier and McCrae, on "Carcinoma of the Stomach in the Young," New York 
Med. Jour., vol. Ixxi., p. 581, 1900. 



THE DIGESTIVE SYSTE.AI. 



503 



The third type, gelatinous carcinoma (Fig. 190, page 318), often 
forms extensive growths and is apt to invade adjacent structures and to 
establish metastases. 

Stenosis of the pylorus and chronic gastritis, adhesions, fistulte, dis- 
tortion of the stomach, x)erf orations, etc., hsemorrhage, suppurative 
inflammation, are among the frequent secondary complications of gastric 
cancer. 

Among the relatively infrequent secondary cancers of the stomach, 
those originating in the breast are proportionately large. ' 

Cysts of the stomach wall have been recorded. ^ 

For recent general bibliography of lesions of the stomach, see Tliorel, Lubarsch and 
Ostertag's " Ergebnisse, " Jahrg. v. for 1898, p. 142. 



FOREIGN BODIES. 

Among the various foreign bodies which by accident or design may 
be present in the stomach may be mentioned hairs, thread, string, etc., 
which have been swallowed from time to time, usuallj" by hysterical 
women. These may be closely packed together into a large mass nearly 
filling the cavity of the stomach, to which in shai^e it may correspond 
(Fig. 281).^ 

The Intestines. 

Malformations . 

Atresia Ani.— Absence of the anal opening is frequent. This may be associated 
with partial or complete atresia of the rectum or of the colon which may be represented 
by solid cords. Blind terminations of the small intestine 
may occur, or there maj^ be complete closure of the gut. 

Transposition. — The position of the intestines may 
be the opposite to that which is usually found. The 
transposition may affect all the abdominal viscera, or 
only a single viscus is transposed. 

Anomalous Positions of the Colon are not infre- 
quent.* 

DiYERTicuLA. — Intestinal diverticula are most fre- 
quent in the lower part of the ileum. They usually 
spring from the convex surface of the intestine, more 
rarely from its attached border. In the latter case they 
are joined to the mesentery by a fold of peritoneum. 
The diverticulum forms a pouch from one to six inches 
long, of about the same diameter as the intestine, smallest 
at its free extremity (Fig. 285). 

^ For statistics see Welch, reference above. 

^ Schultz has seen a large cyst of undetermined origin. 
Trans. Xew York Path. Soc, 1899-1900. 

^ Such a specimen of gastric hair ball, mentioned 
by Osier, is in the museum of McGill University, and 
another, reported by Findler (see Fig. 284), is in the 
museum of the College of Physicians and Surgeons, New 
York. Jacohson has recently described a case, giving 
bibliography, Med. News, February 16th, 1901. 

■* For bibliography of reported cases see Shober, Am., fkj, 285.— Diverticulum of the 
Jour. Med. Sciences, vol. cxvi., p. 405, 1898. Small intestine. 




504 THE DIGESTIVE SYSTEM. 

Such diverticula do not interfere with tlie functions of the intestines. They occa- 
sionally form part of a hernia. Sometimes the remains of these intestinal diverticula — 
called Meckel's diverticula — form soft, projecting tumors at the umbilicus^ in children. 
Microscopical examination of such tumors often shows the structure of the intestinal 
mucosa and muscularis. If they remain attached by a fibrous cord to the navel, this 
cord may be the cause of incarceration of a portion of the intestines.- 

False Dwerticula. — Not infrequently one finds at autopsies either in the small or 
large intestine diverticula or hernise, which project from the exterior of the gut usually 
near its mesenteric attachment. These consist of the mucous membrane which has been 
crowded through the muscularis and is covered by serosa. These so-called " false di- 
verticula " may be large, but are generally not larger than a pea ; they may be single or 
numerous (Fig. 286). The}^ as a rule cause no functional disturbance, but may, through 
the accumulation of faecal material within them, be the seat of perforation. ^ 




Fig. 286.— Multiple False Diverticula of the Intestine. 

Cloaca. — The rectum may open into the bladder, urethra, or vagina. Thus 
cloacae are formed which are often associated with other malformations of the abdomi- 
nal wall, intestines, and generative organs. 



Incarceration. 

1. The most common form is that in which a portion of intestine is strangulated by 
a fibrous band. Such fibrous bands are the result of peritonitis or may be of foetal ori- 
gin. They pass from the intestines to the abdominal wall, or from one part of the in- 
testines to another. The intestine becomes in some way caught under one of these 
bands and is compressed by it. The stricture thus produced may lead to a gradual 
accumulation of faeces in the intestine above it, and may last for a long time before 
death ensues. In other cases the stricture interferes at once with the circulation of the 
blood; the intestine is intensely congested, becomes gangrenous, and death takes place 
with the symptoms of general peritonitis. 

2. A portion of intestine becomes caught in some abnormal opening in the mesen- 
tery or omentum, or in the foramen of Winslow, or between the two layers of the 
mesentery. We have seen a case in which twelve feet of intestine had passed through 
a small opening in the mesentery. 

3. A coil of intestine makes a half turn at its base, so that the two sides of the 
loops cross at its base. In this wa}^ the lumen of the intestine is completely closed and 

^For bibliography of umbilical tumors see Giannettcmo, Arch. sren. de Med., t. iii., 
p. 65, 1900. 

^For bibliography see Reinman, Proc. Path. Soc. of Philadelphia, new ed., vol. i., 
p. 193, 1898. 

s Consult Fischer, "False Diverticula of the Intestine," Jour. Exp. Med., vol. v., p. 
333, 1901, bibliography. 



THE DIGESTIVE SYSTEM. 505 

the vessels are compressed, so that congestion, peritonitis, and gangrene result. This 
form of incarceration is most frequent in the ascending colon. In the small intestine 
it may occur when the gut is fixed by old adhesions. 

4. A portion of the intestine, with its mesentery, makes one or more complete turns 
on itself, closing the canal and compressing the vessels. 

5. A portion of the intestine makes a half or entire turn about its longer axis. 
This is very rare, and only occurs in the colon. 

6. The mesentery of a part of the intestine is long and loose, in consequence of a 
dragging down of the intestine b}^ a hernia or by habitual constipation. The portion 
of intestine thus permitted to hang down is habitually filled with faeces, and by its press- 
ure on some other part of the intestine produces an incomplete stricture. 



Intussusception. 

This change of position consists in the invagination of one portion of intestine in 
another portion. Usually this takes place in the direction of the peristaltic movements, 
from above downward ; more rarely in the opposite direction. 

The parts are found in the following condition: There are three portions of intes- 
tine, one within the other. The inner portion is continuous with the intestines above 
the intussusception ; its peritoneal coat faces outward. The outer portion is continuous 
with the intestine below ; its peritoneal coat also faces outward. The inner portion is 
turned inside out, its mucous membrane is in contact with the mucous membrane of 
the outer portion. In rare cases the intussusception is complicated by the invagination 
of a second portion of intestine in the inner tube, and even by a third intussusception 
into the second one. These changes occur both in the large and small intestine; most 
frequently the lower part of the ileum is invaginated in the colon. The invaginated 
portion may be from a few inches to several feet in length. The lesion is most fre- 
quently found in early childhood. 

The intussusception, by the dragging and folding of the mesentery which it in- 
volves, maj^ lead to intense congestion of the parts, and even to large haemorrhages be- 
tween the coats of the intestine. The congestion may induce fatal peritonitis, or gan- 
grene of the intestine, or chronic inflammation and adhesions, and the patient may live 
for a considerable time with symptoms of stricture. In other cases the invaginated por- 
tion of intestine sloughs, the outer and inner portions become adherent, and the patient 
recovers, with or without stricture. 

Besides this grave form of intussusception we often find, especially in children, one 
or more small invaginations not attended with congestion or inflammation. These are 
agonal or are formed immediately after death. 



Dilatation of the Colon. 

This may be congenital or acquired and is sometimes excessive.* 

WOUNDS— RUPTURES. 

Penetrating wounds of the intestine usuallj' prove rapidly fatal, 

either from shock or from peritonitis. Sometimes, however, the wound 

becomes closed by the formation of adhesions with the neighboring 

parts. Sometimes the wound in the intestines becomes adherent at the 

position of the wound in the abdominal wall, and an intestinal fistula is 

formed. 

^ See Fitz, Am. Jour. Med. Sciences, vol. cxviii., p. 125, 1899, bibliography; also 
Griffith, Trans. Assn. Am. Phys., vol. xiv., p. 1, 1899. 



506 THE DIGESTIVE SYSTEM. 

Euptiire of the small intestine is not infrequently produced by severe 
blows on the anterior abdominal wall. It is noticeable that such blows 
may not produce marks or ecchymoses of the skin. Such ruptures usu- 
ally prove fatal very soon, but sometimes the patient lives several days 
and the edges of the rupture undergo inflammatory changes. 

Strictures of the intestine are sometimes followed by rupture of the 
dilated intestine at some point above the stricture. 



DISTURBANCES OF THE CIRCULATION— HAEMORRHAGE. 

Hypersemia of the intestine may be inflammatory in character or it 
may be associated with disturbance of the portal circulation. Under 
both of these conditions ecchymoses may occur. Pigmentation may fol- 
low large or small interstitial haemorrhages. 

As a result of embolism or thrombosis of the mesenteric vessels, hsem- 
orrhagic infarctions may occur, sometimes involving considerable portion 
of the gut. ' Haemorrhage into the lumen may follow, or gangrene, or 
inflammation. The latter processes are readily induced in the injured 
regions by the bacteria constantly present in the intestinal contents. 
Septic emboli may induce suppurative inflammation in the mesentery 
and in the wall of the intestine. 

Intestinal haemorrhage may occur in venous congestion, as in certain 
forms of cirrhosis of the liver. It may follow ulceration, in typhoid 
fever, in chronic colitis, in malignant tumors, etc. ; it may accompany 
infarction. 

DEGENERATION. 

Amyloid Degeneration may be associated with a similar process else- 
where in the body. The iodin test may reveal the existence of this 
alteration in the villi of the small intestine. 



INFLAMMATION. 

In^flammation of the Small Intestine. (Enteritis.) 

Acute Catarrhal Enteritis. — This may occur under conditions similar 
to those inciting catarrhal inflammation in the stomach. It may be local 
or general and may be associated with similar processes in the stomach 
and colon. In ptomain poisoning the lesions are often severe. Com- 
paratively mild forms of the lesion may predispose the intestine to the 
incursions of intestinal bacteria and the development of more severe 
forms of destructive lesions. The mucosa may be reddened or ecchy- 
mosed, and covered with mucus mingled with degenerated epithelium 
and leucocytes. The epithelium may be degenerated and peeled off (Fig. 

^ For a fuller consideration of thrombosis of the mesenteric veins consult WelcJi, 
Allbutt's "System of Medicine," vol. vi., p. 218. 



THE DIGESTIVE SYSTEM. 507 

287), and the cylindrical cells may be distended with mncus formed 
within them — ^ ^beaker cells. '^ 

The solitary and agminated lymph-nodnles may be swollen from 
hyperplasia. {Bee Lesions of the Lymph-nodes, page 364.) When this 
hyperplasia is marked (Fig. 288), the lesion is often called follicular or 
nodular enteritis, and erosions and nlceration may occnr (Figs. 296 and 
297). For hyperplasia of the lymphoid tissue of the intestine in typhoid 
fever see page 204. 

Chronic Catarrhal Enteritis. — This may follow the acute form or occur 
independently. It often accompanies many forms of chronic disease of 
the heart, kidneys, lungs, etc. The mucous membrane may be covered 
with mucus; ecchymoses, erosions, and pigmentation are frequent. 
There is hyperplasia of the interglandular 

tissue of the mucosa and the submucosa. In ^ ' . r ^^"^ ' ^ <-« 

this way there may be atrophy of the glands -^ ' 

and the miicous membrane may be thin and , ' - ^ ., ,\ 

fibrous. The muscularis may also be in- ' / 1 

volved and atrophied. The submucosa and ^ ^ A 

the muscular layer may on the other hand be ^ \ "' ^ ^ "^ 



. / 



thickened from the new-formed fibrous tissue. 

Pseudo-membranous Enteritis may occur in :' \ \ ^W\i< 

connection with a similar condition in the ^' - \ c: i ^ ^m- f'/ 

colon, in infectious diseases, in chronic dis- .' , / ' 

eases of the liver and kidney ; in cachectic 
conditions, or as the result of the ingestion 
of irritant poisons. The mucous membrane ,■ ' 
may be the seat of superficial necroses, some- :, '; , 
times in patches, and the pellicle may consist ^ ^ vf^^ - - - 

largely of mucus with necrotic epithelium. no. 287.-acute catarrhal en- 
Fibrin may be iDresent and fibrin and extra- teritis. 

vasated leucocytes and serous fluid may in- showing the open end of one of the 

■fiH f fVi K tubular glands with exfoliating and 

nitrate tne StlDmUCOSa. disintegrating epithelium. 

Exudative or Suppurative Enteritis is rare. 
Purulent foci, usually metastatic in origin, may form in the wall of the 
intestine. A more diffuse suppuration may follow infection after ob- 
struction or strangulation.^ 

Tuberculous Enteritis.— The lymph-nodules and Peyer's patches are 
often involved in intestinal tuberculosis and often ulcerate (Fig. 289). 
Miliary tubercles may be present with cheesy degeneration (Fig. 290) 
and the subperitoneal lymphatic vessels are often involved and may ap- 
pear as white, nodular, branching, slightly elevated cords, running around 
the gut (Fig. 291). Tuberculous tilcers are apt to extend most rapidly 
in a direction transverse to the axis of the gut (Fig. 292), differing in 
this respect from typhoid ulcers (see page 206). But to this there are 
frequent exceptions. Tuberculous ulcers rarely perforate. (See for 
other forms of tuberculosis of the intestine page 515.) 

'For reference to bacterial excitants of enteritis see footnote, p. 514. 



508 



THE DIGESTIVE SYSTEM. 



Syphilitic Ulcers, originating in the lymphatic strnctures, are some-^ 
times found in infantile syphilis. 

Duodenal Ulcers may be tuberculous or may follow extensiye burns. 



^'H 



Fig. 288.— Nodular Enteritis. 
From the intestine of a child. 

In the latter case their mode of origin is obscure. They may occur under 
a variety of other conditions. ' 

Other Forms of Ulcers. — The solitary and agminated lymph-nodules 
frequently undergo hyperplasia, in infectious diseases, after extensive 
burns, in various forms of inflammation of the intestine. Hyperplasia 
of the lymphatic tissue — see above — with ulceration is especially frequent 
in children. 

Anthrax Infection of the Intestine (Mycosis Intestinalis), — The anthrax 
bacillus may find lodgment in the intestinal mucous membrane either by 




Fig. 389,— Tuberculous Ulcers of the Small Intestine. 

In the larger ulcers the mucous membrane is almost entirely gone, leaving the muscularis exposed at the 

bottom. 



the ingestion of food containing the germ or by metastasis through the 
blood from some other seat of infection, especially the skin. 

The intestinal lesions are most apt to occur in the small intestines and 

^ For a study of cUiodenal ulcers see Weir, Medical Record, May 5tli, 1900, bibli- 
ography. 



THE DIGESTIVE SYSTEM. 



509 



iu tlie upper part of the colon. The mucous membrane is studded with 
larger and smaller brown or black frequently elevated patches, or areas 



/y ^ - 



' ^i^t^ 



Fig. 290.— Section of a Tuberculous Ulcer of the Small Intestine. 

Showing tubercle tissue with miliary tubercles and caseation at the bottom of the ulcer. There are miliary 
tubercles beneath the serosa. CSee Fig. 291.) 

of local congestion, or haemorrhage, or necrosis. The mucous membrane 
near the inflammatory and necrotic foci may be oedematous. Hyper- 

J . 1 . ■ J i «'ill l illMk>... 




Fig. 291.— Subserous Tubercles Following the Lymph-tessels at the Botto^j of a Tuberculous 

Ulcer of the Small Intestine. 

plasia of the spleen and lymph-nodes is apt to accompany the intestinal 
anthrax. The anthrax bacillus mav be found about the seat of local 




Fig. 292.— Tuberculous Ulceus of the Small Intestine. 
Showinir the extension of the ulcers in a direction transverse to the axis of the gut. 



510 THE DIGESTIVE SYSTEM. 

lesion in the intestine, in the associated lymph-nodes, and when second- 
ary to local infection elsewhere it may be found in the primary lesion 
and in the blood. 

It is believed that other forms of bacteria may cause intestinal lesions, 
somewhat similar to those of anthrax, but the researches in this direction 
are not yet sufficiently numerous to permit of very definite statements. 

Inflammation of the Large Intestine. (Colitis.) 

The mucous membrane of the large intestine is frequently the seat of 
acute and chronic inflammatory and necrotic processes known clinically 






^;- 



/i' 



;•!/•■ 









.1% 












.1 i/:i;f 



:'£ !■■■ • I- -5' ■•' 'i I 



Fig. 293.— Acute Catarrhal Colitis. 



^ 



Tbe epithelium of the tubular glands, especially near their mouths, is forming an excessive amount of 
mucus with destruction and exfoliation of the cells. The tubules are dilated with mucus which covers the 
surface. The mucosa at the right is necrotic and forms the edge of an ulcerated area. 

as dysentery. ' The rectum is most often involved, but sometimes the up- 
per part of the colon and sometimes the whole colon is affected. 

Acute Catarrhal Colitis. — This process is frequently limited to the lower 
end of the colon and i)resents several types. There may be an increased 
production of mucus, which coats the surface of the mucous membrane 
and is mixed with exfoliated and fatty or disintegrated epithelium and 
red blood cells. The surface epithelium may be degenerated and ex- 
foliate, many ^^ beaker cells" being present, indicating the source of over- 

^ The classification of tliese lesions is with our present knowledge unsatisfactoiy, 
and the enumeration of various phases is largely based upon morphology. In the so- 
called tropical dysentery, however, the nature of the excitant is taken into the account. 
Consult for a special study of forms of colitis seen in New York Delafield, Am. Jour. 
Med. Sciences, vol. cxiv., p. 401, 1897. 



THE DIGESTIVE SYSTEM. 



511 



production of mucus (Fig. 293). The mucous membrane may be con- 
gested and infiltrated with serum and leucocytes. Again, with conditions 
similar to those just described, there may be a i)urulent exudate in the 
mucous membrane. There is a form of catarrhal colitis in which there 
is a more or less extensive formation of new connective tissue between 
the glands and in the submucosa. Finally, there may be small or exten- 
sive ulceration in the involved areas of the mucosa. 

Acute Infectious Colitis (Tropical Dysentery) is of frequent occurrence 
in warm countries and is often epidemic. In one group of cases («) the 
disease is incited by protozoa — amoebae coli; while in the other (&), bac- 




FlG. 294.— AMOEBIC COLITIS. 

Showing amoebae in the submucous fibrous tissue. 



teria, some apparently of the colon bacillus group, and possibly others, 
are believed to be the excitants. 

(«) Amcebic Colitis. — This form of colitis is incited by the presence 
in the wall of the intestine of the Amoeba coli. 

The amoebse are found in the gelatinous masses which are common in 
the stools. They are of rounded shape, and, when alive, change their po- 
sition and shoot out and retract little projections (pseudopodia). Their 
outer portion is composed of a pale hyaline or homogeneous substance ; 
the inner contains vacuoles and is more refractive (see page 128). 

In the colon the amoebae are found in the connective -tissue coat (Fig. 
294) and in the floors of the ulcers. 

Amoeba excites at first a moderate exudative and productive inflam- 
mation followed by necrosis. Thus ulcers are formed. The ulcers may 
be superficial or deep, sometimes extending to the x)eritoneum ; they en- 
large by infiltration and necrosis at their edges, so that extensive de- 
struction of the mucous membrane may occur. The amoeba may be 
present in the connective tissue at the base or sides of the ulcers. I^ot 
infrequently, owing to bacterial infection from the intestinal contents, 
varying degrees of supx)urative inflammation may comi)licate the lesion. 

Necrotic and suppurative processes may be set up in the liver (see 



512 THE DIGESTIVE SYSTEM. 

page 544) and in the right Inng, and in these lesions the amoeba may be 
found. 

(5) Acute Infectious Colitis with Bacterial Excitaistts. — 
dimerous studies have been made of the micro-organisms occurring in 
connection with tropical dysentery, and there appears to be an im]3or- 
tant group of cases in which the amoeba coli is not concerned and in 
which bacilli, pathogenic for certain animals and somewhat resembling 
the typhoid and the colon bacilli, have been found. The more recent 
and important bacterial and morphological studies on this form of colitis 
are those of Shiga in 1897 and of Flexner in 1899.' 

Bacillus pyocyaneus has been repeatedly found in the discharges in 
cases of dysentery as well as in other intestinal disorders under condi- 
tions which justify the conjecture that it is sometimes at least an excitant 



' 'J ji ' '' 












FiG. 295.— Nodular Colitis -Follicular Colitis. 
Showing commencing necrosis of the mucosa over the hyperplastic lymph-nodule. 

of intestinal inflammation and necrosis.^ Streptococcus pyogenes has 
been repeatedly found in association with colitis. 

Nodular Colitis (Follicular Colitis). — In many cases of catai^rhal and 
croupous inflammation of the colon the solitary follicles (lymph -nodules) 
become more or less swollen and necrotic. Besides these cases, however, 
there are others in which the changes in the nodules form the principal 
part of the lesion, while the catarrhal or croupous inflammation is but 
slightly developed. The lesion is similar to that in nodular enteritis. 
The nodules are first swollen — hyperplastic — (Fig. 295), then necrotic, 
then slough away and leave little circular ulcers with overhanging edges 
(Fig. 296). These ulcers are usually numerous (Fig. 297) and maybe 
scattered over a large part of the colon. The ulcers are apt to show but 
little disposition to heal, and the acute colitis often becomes chronic. 

^ For details of these studies consult Flexner, " On the Etiology of Tropical Dysen- 
tery," Phila. Med. Jour., vol. vi., p. 414, 1900. 

■^See Lariigau, Jour. Exp. Med., vol. iii., p. 595, 1898. 



THE RESPIRATORY SYSTEM. 481 



The Mediastinum. 



Inflammation. — Suppurative inflammation ma}^ occur either in the anterior or 
posterior mediastinum. It may be caused by fractures, caries or necrosis of the ster- 
num and vertebra}, by perforation of the oesophagus, by suppuration of the lymph- 
nodes, by pleurisy, or may occur without discoverable cause. 

The pus may infiltrate the connective tissue, or may form abscesses which may 
attain a large size. The inflammation may extend to the pleura or the pericardium, 
the abscesses may displace the heart, the lungs, or the sternum ; or they may perforate 
through the skin, into a pleural cavity, the oesophagus, the trachea, or a bronchus/^ 

A few cases of chronic inflammation of the tissues of the mediastinum have been 
reported — chronic mediastinitis.^ 

Tumors. — The most common form of new growth in the mediastinum is that 
known by the names of lymplioma, lympTio-sarcoma, and lymph-adenoma. 

These tumors are confined- to the mediastinum, or they are associated with similar 
growths in other parts of the body in the disease called "pseudo -leukaemia." Persons 
between the ages of twenty and thirty years seem to be the most liable to the growth, 
but it is also not uncommon in children. 

It begins in the lymph nodes in the mediastinum, and at the root of the lung. 
It increases at first slowly, then more rapidly, and gradually infiltrates the adjoining 
tissues. In this way the walls of the trachea, bronchi, and aorta, the pericardium, the 
pleura, and the lung, become infiltrated with compression of the surrounding organs. 

The growth is composed of a fibrous stroma associated with small round cells, the 
relative quantity of cells and stroma varying in the different cases. 

Besides this form of tumor there may also occur in the mediastinum tumors similar 
to those which grow in the pleura and behind the peritoneum — tumors which resemble 
both the sarcomata and carcinomata, and which it is difficult to classify. Aberrant 
thyroid-gland tissue may be found in the mediastinum. 

Complex tumors belonging among the foetal inclusions or teratomata are of occa- 
sional occurrence in the anterior mediastinum. ^ They may contain bone, cartilage, con- 
nective tissue, muscle, hairs, skin, etc. Cysts sometimes lined with ciliated epithelium 
mav form in such tumors.'* 



442. 



^ For tuberculous lesions of the tracheo-bronchial lymph-nodes see reference, p. 

'^Whipham, Lancet, 1899, vol. i., pp. 882, 947, bibliography. 
^See Mandlebaum, Am. Jour. Med. Sciences, vol. cxx., p. 64, 19C0. 
'^ Consult Rare, " Tumors of the Mediastinum, " Philadelphia, 1889 ; also Zahn, Vir- 
chow's Archiv, Bd. cxliii., pp. 170 and 416, 1896. 
31 



CHAPTER VII. 

THE DIGESTIVE SYSTEM. 

The Mouth. 

Malformations. 

Malformations of the lips and cheeks are usually associated with defective forma- 
tion of the bones of the mouth. The entire process is generally due to an arrest of de- 
velopment. 

1. The lower jaw is absent; the upper jaw and hard palate are small and imper- 
fectly formed; the temporal bones nearly touch in the median line. The lower part of 
the face is, therefore, wanting; the mouth is absent, or small and closed posteriorly; 
the tongue is absent. Such a malformation is rare ; the foetus is not viable. 

2. The face remains in its early foetal condition of a large cleft ; the mouth and nose 
form one cavity ; the orbits may be united in the same cavity. The foetus is not viable. 

3. There is a cleft in the upper lip, upper jaw, and hard palate. The cleft corre- 
sponds to the point of junction of the processes of the superior maxilla with the inter- 
maxillary bone. There may be one cleft or two, one on either side of the intermaxillary 
bone. The cleft involves the lip alone, or the lip and superior maxilla, or the lip, max- 
illa, and palate. There may be a single or a double cleft in the palate, and the cleft 
may involve eithei- the hard or soft palate, or both. If there are two clefts of the lip 
and maxilla the portion of lip and bone between them may be small, or entirely absent 
so as to leave a large open space. The soft palate may be entirely absent. This isa 
common malformation and does not endanger life. 

4. Earely we find a cleft involving the middle of the lower lip, and sometimes ex- 
tending into the inferior maxilla. 

5. Either the inferior, the superior, or both maxillary bones may be abnormally small. 

6. The edges of the lips ma}^ be partly or completely joined together. The open- 
ing of the mouth may be only a round hole. 

7. The lips may be absent or imperfectly developed. 

8. The corners of the mouth may be prolonged by clefts in the cheeks nearly to the 
ears. 

INFLAMMATION. (Stomatitis.) 

Catarrhal Stomatitis is most frequent in children and occurs with a 
great variety of local and general disturbances. 

During life the congestion and swelling of the mucous membrane may 
be well marked and there are often white patches, produced by the death 
of the superficial epithelial cells. There may be an increased production 
of mucus, or, instead of this, the entire mucous membrane is unnaturally 
dry. In addition to hypersemia and local oedema there may be prolifer- 
ation, exfoliation, and degeneration of the epithelium. 

Extravasated leucocytes may infiltrate to a moderate degree the 
stroma of the mucous membrane and appear upon its surface. Small, 



THE DIGESTIVE SYSTEM. 483 

clear vesicles may form beneath the epithelium from the collection of 
serous exudate. 

Croupous Stomatitis is incited by local irritants, by local infection, or 
by the extension of the same form of inflammation from the pharynx ; it 
frequently occurs with diphtheria and other infectious diseases. 

Portions of the mucous membrane are swollen and congested, and 
covered with a false membrane. This false membrane is composed of a 
thickened layer of epithelium in the condition of coagulation necrosis, 
and of fibrin and pus in variable relative quantity. The stroma of the 
mucous membrane may be infiltrated with pus and fibrin, and portions 
of it may become necrotic. 

Aphthous Stomatitis. — In this condition small whitish projecting 
patches surrounded by a zone of hyperaemia may form upon the mucous 
membrane. These consist of a more or less fibrinous exudate beneath 
the epithelium which may exfoliate, leaving small ulcers. 

Ulcerative Stomatitis. — This form of stomatitis is apt to occur in ill- 
nourished children or in young adults, in scurvy, or in mercurial poison- 
ing. It usually begins at the margin of the gums of the lower jaw and 
extends to the cheeks and tongue. The affected parts are swollen and 
coated with a grayish, soft pellicle composed of bacteria and necrotic tis- 
sue. The gums may be destroyed around the teeth, and these may fall 
out. The surrounding soft parts are swollen, and there may be necrosis 
of the jaws. 

In Noma or Gangrenous Stomatitis similar changes may be associated 
with extensive gangrenous destruction of the cheeks. This most often 
occurs in young children in connection with measles, scarlatina, or ty- 
phoid fever. It has been claimed that a special micro -organism is the 
excitant of this disease, but this has not yet been proven. 

Thrush. (Soor; Parasitic Stomatitis.) — In ill -nourished children or in 
adults suffering from chronic disease a fungus related to the yeasts — 
oidium albicans — may grow among the epithelial cells of the mouth, form- 
ing white membranous patches. These may involve large areas of the 
mouth and pharynx and may extend to the oesophagus or upper respira- 
tory passages. 

Phlegmonous Stomatitis. — Exudative inflammation of the mouth may 
result from infected wounds, in connection with erysipelas or suppura- 
tive or other infectious process near the mouth. Various pyogenic bac- 
teria may be its excitants. 

Chronic Stomatitis. — This may follow acute catarrhal or other inflam- 
matory processes, and may be due to persistent irritation, for example, 
from the use of tobacco. Owing to hyperplasia of the epithelium and 
submucous tissue white patches of varying extent may form on the 
tongue or elsewhere — leiicoplaMa biiccaJis. These through excessive in- 
crease in the epithelium may project in wart-like form from the surface 
— ichthyosis. 

Tuberculous Stomatitis commences with the formation of miliary 
tubercles or of larger tuberculous masses in the stroma of the mucous 



484 THE DIGESTIVE SYSTEM. 

membrane. These masses soon degenerate, soften, and form ragged 
ulcers. 

Syphilitic Stomatitis.— As a result of syphilis there may be produced 
either the so-called mucous patches or gummy tumors. In the mucous 
patches the epithelial layer is at first thickened and the papillae of the 
stroma are swollen and infiltrated with cells (see Fig. 123, page 233 and 
Fig. 124, page 234). This may be followed hj desquamation of the 
epithelium and ulceration. 

TUMORS. 

Fibroma, lipoma, and enchondroma have been seen in a few cases in the 
lips. When they appear in the mouth they usually grow from the bones. 

Papilloma occurs most frequently at the edges of the lips, but is 
also found on the gums, the floor of the mouth, and the cheeks. They 
are formed of hypertrophied papillse, covered with thickened epidermis. 
They often ulcerate. 

Angioma, either congenital or developed after birth, occurs in the 
lips. 

Adenoma may be formed in the mucous membrane covering the 
mouth, lii)s, and soft palate. The tumors are rounded, usually small, 
sometimes as large as a hen's egg. They may be situated in the thick- 
ness of the mucous membrane, or project in a polypoid form. 

Carcinoma is of frequent occurrence and is usually of the epithelioma- 
tous form. Such tumors may form at any part of the mucous membrane 
of the mouth, but often begin in the edge of the lower lip as a result of 
persistent irritation, as in pipe smokers. 

They may originate in an ulcerating papilloma, or as a flat, super- 
ficial growth from the deeper layers of the epithelium, or as deep nod- 
ules starting in the mucous glands. They are composed of large masses 
of epithelial cells, closely packed together, often forming nests, and 
arranged in anastomosing tubular masses. The stroma surrounding 
these masses is infiltrated with cells. In a few cases the infiltration of 
the stroma with small round cells may be very marked, so marked that 
the epithelial growth may be obscured. The new growth may increase 
in size, ulcerate, infiltrate the adjacent tissues, and may give rise to 
metastatic tumors. 

Cysts. — Dermoid cysts and cysts of the embryonal branchial clefts 
may involve the mouth.. 

The Tongue. 

Malformations. 

Absence of the tongue may be associated with the extreme defects of development 
of the face ah-eady mentioned. 

The anterior portion of the tongue may be absent while its base remains. The 
lower jaw is then small. 

Tlie tongue may be partly or completely adherent to the floor of the mouth. The 



THE DIGESTIVE SYSTEM. 485 

frenulum may be abnormally short, or may extend to the tip of the tongue. In rare 
cases the sides of the tongue are adherent, or its upper surface may be adherent to the 
roof of the mouth. 



HYPERTROPHY AND INFLAMMATION. 

Macroglossia, or hypertrophy of the tongue, is almost always a con- 
genital lesion, and is especially common in cretins. The tongue may be 
so large that it protrudes through the lips. The lips maj^ also be simi- 
larly enlarged. There is hyx)erplasia of the fibrous and other tissues of 
the tongue, and in addition to this there may be a dilatation of the lym- 
phatic vessels. 

Infiammations of the tongue may be associated with similar changes in 
the mouth, or may occur by themselves. 



TUMORS. 

Cysts. — The most common forms of cysts are the sacs beneath or partly 
in the substance of the tongue — ranula. They are formed by dilatation 
of the ducts of the mucous glands, or of the submaxillary and sublingual 
glands. Amyloid tumors of the tongue have been reported. ' 

Lipoma and fibroma are rare. They form nodules in the substance 
of the tongue or project in a polypoid form. Composite tumors, com- 
posed largely of fat, are found on the tongue as a congenital condition. 

Angioma. — Cavernous vascular tumors are found in the substance of 
the tongue and projecting from its surface. 

Sarcoma is not common in this situation, but may occur both in chil- 
dren and in adults. Carcinoma, usually of the epitheliomatous type, may 
originate in the tongue or may extend to it from the adjacent tissues. 



MICRO-ORGANISMS IN THE MOUTH. 

Micro-organisms of various forms— bacteria, moulds, and yeasts — are 
always present in the mouth, often in enormous numbers. They are for 
the most i)art not of significance save for the putrefactive x>rocesses 
which they initiate and maintain in mouths not iDroperlj^ cleansed. On 
the other hand, Staphylococcus and Streptococcus pyogenes and the pneu- 
mococcus are of frequent occurrence in the mouths especially of those 
who live in towns and crowded dwellings, and while usually harmless, 
they may under favorable conditions become excitants of serious disease. 

The tubercle bacillus may be present in the mouth as well as in the 
nose of those who care for uncleanly consumptives. 

The fungus of aphthse (soor), and leptothrix, which under usual 
conditions are not harmful, may incite serious local disease. 

^See Schmidt. Virch. Arch., Bd. cxliii., p. 369, 1896, bibliography of amyloid 
tumors in general. 



486 



THE DIGESTIVE SYSTEM. 



The so-called Mycosis pharyngis is apparently due to the growth in 
susceptible persons of a form of leptothrix not yet thoroughly studied, 
on account of the technical difficulties in the way of its artificial cultiva- 
tion. ' 

The Pharynx. 

Malformations . 

Branchial Fistula and Cysts.— When, as not infrequently occurs, the embry- 
onal gill clefts do not properl}' close, fistulce may remain. These may in rare cases be 
complete, so that an opening exists from the pharynx, larynx, or trachea to the side of 
the neck. More frequently, however, these fistulse are incomplete and shallow, and 



fmmm 




Fig. 2T4.— Section of the Wall of a Branchial Cyst of the Neck. 

Formed from the imperfect closure of an embryonal gill cleft. The cyst is lined mth ciliated epithelium 
and the wall is largely formed of difEuse lymphoid tissue. 



open either inward into one of the above-named organs or outward on to the neck. 
Small portions of the gill clefts may persist without external openings, and from these 
subcutaneous cysts of the neck are often developed. Or a portion of the cleft may be 
cut off, forming a cyst, while the fistula persists with its external opening. 

The walls of these fistulce and cysts may be covered with mucous membrane having 
cylindrical or flattened or ciliated surface cells. Or, when formed from the outer clefts, 
they may be lined with skin. 

Not infrequently the walls of these cysts and fistulse are embedded in lymphatic 
tissue, which may be diffuse or gathered in nodular form (see Figs. 274 and 275). '^ 

Diverticula of the pharynx have been observed. 

^ For a resume with bibliography of the bacteria found in the mouth as well as in 
other parts of the body under normal and pathological conditions, see Mace, " Bacteriol- 
ogie," 1901, p. 1140. 

'^ For bibliography of branchial cysts and fistula? see Coplin, Proc. Path. Soc. of 
Philadelphia, ne"w series, vol. iv., p. 109, 1901. 



THE DIGESTIVE SYSTEM. 



487 



INFLAMMATION. (Pharyngitis.) 

Catarrhal Pharyngitis is usually associated with the same forms of 
inflammation iu the mouth and has similar characters. 

In catarrhal inflammation involving the tonsils and those portions of 
the pharynx richly sui3plied with the so-called submucous adenoid — 
lymphoid — tissue, leucocytes may in considerable numbers pass through 
the thin epithelial layer and mingle with the exudate upon the exposed 
surface. 

In chronic inflammation of the pharynx there may be a large and 
permanent hyperplasia of ' the lymphoid tissue, with more or less dense 




Fig. 275.— Section of the Wall of a Branchial Cyst of the Neck. 

This cyst, like that shown in Fig. 274, has much lymphoid tissue in the wall, hut nodular in character ; 
while the epithethial lining is squamous in type. 



fibrous tissue, leading to ditfuse or circumscribed nodular or peduncu- 
lated masses of vascular ucay tissue in the vault or elsewhere in the 
pharynx, called '^ adenoids. ^^ ' 

Phlegmonous Pharyngitis may occur with inflammations of the mucous 
membrane, with caries of the cervical vertebrae, with inflammation of 
the cervical and parotid glands, with periostitis of the cranial bones, or 
it may occur independently. It may result in swelling and oedema, in 
induration, or in suppuration. It is most important when it affects the 
posterior wall of the pharynx and forms retro -pharyngeal abscesses. 
Such abscesses may cause death by sutfocation. 

Diphtheritic Pharyngitis is that form of pseudo -membranous or croup- 
ous inflammation of which the Bacillus diiDhtheriae is the excitant. The 
general characters of the diphtheritic infection have been considered in 
an earlier part of this book. The local process often affecting the fauces, 

^ For a study of the uvula in various abnormal conditions see Hoen, Jour. Exp. 
Med., vol. iii.. p.%549, 1898. 



488 THE DIGESTIVE SYSTEM. 

pharynx, and tonsils, may involve the mouth as well as the larynx and 
trachea. (For details of the local lesion see page 235. ) 

Tonsillitis. — The tonsils may share in the inflammatory processes of the 
pharynx or be independently affected. The structural characters of the 
tonsils render them liable to infection and involve certain peculiarities in 
the lesions.' 

In Follicular Tonsillitis the swollen organ shows upon section an 
increase in the number of the lymphoid cells of the nodules and an 
hyperplasia of the endothelium of the reticulum. These new-formed 
and often exfoliated endothelial cells are similar to those found in the 
lymph-nodes in general in the presence of bacterial or other toxic sub- 
stances. There may be an increase in the cells of the stroma of the ton- 
sil. The epithelial cells of the surface and the cryi)ts may increase in 
number and exfoliate. Epithelial cells and leucocytes and other forms 
of exudate may gather in the crypts or over the surface of the tonsil, 
forming white plugs or a whitish pellicle. ^ 

In Exudative Tonsillitis (suppurative or phlegmonous tonsillitis, 
quinsy) there are in addition to hyperplasia and catarrhal inflammation 
(edematous swelling and suppuration often leading to abscess. ^ 

Acute inflammation of the pharynx and tonsils is usually infectious 
in character, and may be due to various forms of pyogenic and other 
organisms. Thus in tonsillitis and other forms of acute angina, the most 
common micro-organisms concerned are Streptococcus and Staphylo- 
coccus pyogenes, the pueumococcus, and the Micrococcus tetragenus. 
Many other forms have been isolated. ' 

In Chronic Tonsillitis (the so-called hypertrophy of the tonsils) 
there is hyperx)lasia of the lymph-nodules with increase in the fibrous 
stroma. The mouths of the crypts may be occluded and distended with 
exfoliated cells and cell detritus ; these may become calcified. " 

Tuberculous Pharyngitis. — Tuberculous inflammation of the pharynx 
may be primary or secondary to tuberculous lesions elsewhere ; ulcers 
may form and the tonsils may be involved. 

The hyperplasise of the pharyngeal mucosa in children, commonly 
called ^^ adenoids, "have been found in a considerable number of cases to 
be tuberculous. Whether in these instances the lesion is tuberculous in 

gin or whether the hyperplastic tissue affords a portal of entry and 

al vulnerability to infection by the tubercle bacillus is not yet clear. ' 

^ Consult DohroicoUM, "Lymph Nodules of the Larynx, (Esophagus, etc.," Ziegler's 
viirage z. path. Anat., Bd. xvi., p. 43, 1894. 

^ See Hodenpyl, "Anatomy and Physiology of the Faucial Tonsils," Am. Jour. Med. 
Sciences, vol. ci., p. 257, 1891; also Packard, Philadelphia Med. Jour., vol. v., 1900, 
pp. 914, 957. 

^Consult for bacteriology of angina Lartigau, Philadelphia Med. Journal, vol. iii., 
p. 899, 1899, bibliography; for a study of acute tonsillitis see Goodale, Jour. Boston 
Soc. Med. Sciences, vol. iii., p. 63, 1899. 

■^For resume of tonsillar calculi with bibliography see Eohinson. British Med. Jour., 
1899, vol. i., p. 14. 

'" For a study of pharyngeal tuberculosis see Theisen, Journal of American Medical 
Association, vol. xxxiii., p. 382, 1899, bibliography. 

Also for a study of the tonsils as portals of entry of tubercle bacilli see i\ Sdieiher, 



THE DIGESTIVE SYSTEM. 



489 



The possibility should be borne in mind that from tuberculous ^'ade- 
noids ^' tubercle bacilli may pass through the lymph -channels to the 
bronchial lymph-nodes, and that the pharynx may thus be a more impor- 
tant portal of entry in tuberculosis than has been hitherto recognized. 



TUMORS. 



Fibromata grow from the periosteum of the bones at the base of the 
skull, and project into the cavity of the i)harynx and posterior nares in 




Fig. 276.— " Adexoid " Polyp of Phartxx. 

the form of large polypoid tumors. Soft polypoid tumors, consisting 
largely of loose succulent connective tissue and lymphatic tissue and 
often called " adenoid polyps" (see Fig. 276), are of frequent occurrence. 
They are usually to be regarded rather as hyperplasiae than true tumors. 
Hairy polyps of the pharynx have been described by Arnold ' and others. 

Ziegler's Beitr., Bd. xxvi., p. 511, 1899; also Friedemann, ihid., Bd. xxviii.,p. 66, 
1900. 

For ^ ■ ' '.■'■■''-^graphy on the tonsils see Ullman, Medical News, January 26th. 
1901, p. ] . reference to Grober, p. 436. 

^ Arr, 's Arch., Bd. cxi., p. 176, bibliography. 



490 THE DIGESTIVE SYSTEM. 

The occurrence of cartilage aud bone in the tonsil has been described by 
Stoeltzner. 

Sarcoma, carcinoma/ and various tumors of mixed type are of fre- 
quent occurrence in the pharynx.^ 



The (Esophagus. 

Malformations. 

The oesophagus may be entirely absent, or its lower portion may be present and 
joined to the pharynx by a solid cord; or the pharynx, or the lower part of the oesoph- 
agus, may be continuous with the trachea; or the entire oesophagus may be represented 
by a solid cord. Dilatations of the oesophagus and division of the middle portion of the 
oesophagus into two branches have been observed. 

PERFORATION AND RUPTURE. 

Foreign bodies in the oesophagus may, as already mentioned, perfo- 
rate its wall. Perforation of the oesophagus from without may be pro- 
duced by inflamed bronchial glands, by the extension of cavities and 
gangrene of the lungs, by abscesses in the mediastinum, by abscesses 
accompanying caries of the vertebrae, and by aneurisms of the aorta. 
Eupture of the wall of the oesophagus by violent coughing and vomiting 
has been described, but it seems improbable that this should occur with- 
out some previous local lesion. ^ A few cases of perforating ulcer of the 
oesophagus have been recorded. 

HiEMORRHAGE. 

Aside from injuries, ulceration, etc., haemorrhage may take place 
from the veins of the oesophagus, which, especially in atrophic cirrhosis, 
may be much dilated." 

DILATATION. 

Simple Cylindrical Dilatations of the oesophagus are usually the result 
of 1 r-ug- continued stenosis of the oesophagus or of the cardiac end of the 
- niach, although not nearly all the stenoses are followed by dilatation. 
3 dilatations are formed at first immediately above the stenosis and 
. extend upward. Only in rare cases does the dilatation involve the 
v\ 1iv.1j length of the tube. The entire wall of the dilated portion of the 
oesophagus is thickened, and there may be polypoid growths from the 
mucous membrane. 

^ For a study of carcinoma originating in the branchial cleft see Poioers, Annals of 
Surgery, February, 1898. 

2 For literature of malignant disease of the tonsils consult NeiDman, Am. Jour. 
Med. Sciences, vol. ciii., p. 487, 1892; also Hoi^sell, Beitr. zur. klin. Chirurgie, Bd. xiv. 

^For a study of rupture of the oesophagus see McWeenep, Lancet, 1900, vol. ii., p. 
158, bibliography. 

*See Preble, Am. Jour. Med. Sciences, vol. cxix., p. 263, 1900. 



THE DIGESTIVE SYSTEM. 491 

In rare cases there is cylindrical dilatation of part or of the whole of 
the oesophagus without a stenosis or any discoverable cause. In these 
cases the dilatation is usually greatest near the middle of the oesophagus 
and diminishes upward and downw^ard, so that the oesophagus has a fusi- 
form shape. The dilatation may reach a very considerable degree, the 
walls of the oesophagus are thickened, its mucous membrane may be 
covered with pai^illary outgrowths or ulcerated. 

The Sacculated Dilatations of the oesophagus are of two kinds : those 
due to pressure, and those due to traction. 

The dilatations due to j)ressure are situated in the posterior wall of 
the pharynx, just at its junction with the oesophagus. The smaller sacs 
are from the size of a pea to that of a hazelnut ; the larger sacs may 
reach a large size and hang down between the oesophagus and the verte- 
bral column, the opening into the oesophagus remaining comparatively 
small. It is supi)osed that a limited area of the wall of the oesophagus 
loses its power of resistance against the pressure exercised upon it in 
each act of swallowing ; it then is forced outward by the pressure, and 
so there is formed first a protrusion and then a sac. When a sac is 
formed the food enters it, accumulates there, and the sac becomes larger 
and larger. 

The dilatations due to traction are situated on the anterior wall of 
the oesophagus, at a point nearly corresponding to the bifurcation of 
the trachea. They are of funnel shape, with the small end outward. 
Their length varies from two to twelve millimetres ; the width of the 
opening into the oesophagus is from six to eight millimetres. 

These dilatations are due to inflammation of the parts adjoining the 
oesophagus, especially of the bronchial nodes, followed by adhesions to 
some part of the anterior wall of the oesophagus. These adhesions then 
contract and draw the wall of the oesophagus outward, and in this way 
the dilatations are formed. 

At a later time these sacs may perforate into the bronchi, the lungs, 
the pleural cavity, the pericardium, the aorta, or pulmonary artery. ' 



STENOSIS. 

Congenital Stenosis. — Besides the defects of development of the oesoph- 
agus which are incompatible with life, there may be a congenital stenosis 
of some part of it which causes difficulty in swallowing, but yet does not 
destroy- life. 

Compression Stenosis is not uncommon. Tumors of the neck and 
mediastinum, and aneurisms of the aorta are the usual causes. 

Obstruction Stenosis. — Foreign bodies may be lodged in the oesophagus. 
Tumors may hang down from the pharynx into the oesophagus, or may 
be situated in the wall of the oesophagus. Inflammation of the oesopha- 

^ For bibliography of oesophageal diverticula see BroscJi, Deutsch. Arch, f . klin. 
Med., Bd. Ixvii., p. 44, 1900. 



492 THE DIGESTIVE SYSTEM. 

gus, due to the ingestion of irritating poisons, may induce cicatricial 
stenosis. A few cases of stenosis due to syphilitic inflammation have 
been reported. 

INFLAMMATION. (CEsophagitis.) 

Catarrhal (Esophagitis may be either acute or chronic. The chronic 
form may lead to ulceration, or relaxation and dilatation of the walls, 
or to hyi)ertroi3hy of the muscular coat. 

Pseudo-Membranous (Esophagitis may occur with a similar process in 
the pharynx, with the exanthemata and other severe diseases, or under 
other conditions. It may be diphtheritic in character or due to other 
excitants than the diphtheria bacillus. 

Tuberculous (Esophagitis may occur in generalized miliary tuberculosis 
or by local infection from tuberculous sputa, either with or without 
obvious predisposing local lesion, or through an extension of a tubercu- 
lous i)rocess from adjacent structures. Ulceration is apt to occur.' 

Other Forms of Inflammation of the (Esophagus. — Foreign bodies which 
are swallowed and become fixed in the oesophagus may incite inflamma- 
tion of the mucous membrane and of the adjoining soft parts. Abscesses 
may form around the oesophagus, or destroy the wall of the canal, and 
the foreign body may find its way into the trachea, aorta, or pericardium. 

Inflammation of the submucous tissue of the oesophagus, apart from 
the cases just mentioned, is not common. It may result in abscess or 
the formation of fibrous tissue, causing stenosis. 

Irritating and caustic acids and alkalies may destroy larger or smaller 
portions of che mucous membrane. The necrosed portions are of a black 
or whitish color, surrounded by a zone of intense congestion. If the pa- 
tient recover, the patches of membrane which have been destroyed slough 
and fall off, leaving a surface covered by granulation tissue. As this 
assumes cicatricial characters and contracts, serious stenosis of the 
oesophagus may be produced. 

TUMORS. 

Small Papillomata may occur singly or in considerable numbers 
throughout the entire length of the oesophagus. Large papillary tumors 
are more rare. Small submucous fibromata and lipomata, and leiomyomata 
of considerable size may occur in the oesophagus. Sarcomata are rare.^ 
Adenomata have been observed. 

Carcinoma may originate at any part of the wall of the pharynx and 
oesophagus. The tumor may encircle the tube ; it may remaiii as a flat 
infiltration, or project inward in large, fungous masses. In either case 
it is j)rone to ulceration. The growth may extend up and down the 
oesophagus, and even involve the pharynx or stomach. The ulcerative 

' For bibliograph}^ of tuberculous oesophagitis see Flexner, Johns Hopkins Hospital 
Bulletin, vol. iv., p. 4, 1893; and also Cone, ibid., vol. viii., p. 229, 1897. 

^'Limngood, Johns Hopkins Hosp. Bull., vol. ix., p. 159, 1898, bibliography. 



THE DIGESTIVE SYSTEM. 493 

process may extend outward so as to lead to jDerf oration into the air 
passages, the lungs, pleurae, pericardium, and large blood-vessels. The 
new growth may extend outward and infiltrate the surrounding soft parts, 
so that the oesophagus is surrounded by large, solid, cancerous masses. 
Metastatic tumors are also sometimes formed. 

Cysts. — Small retention cysts of the follicles of the mucous membrane 
are sometimes found. Larger cj^sts of the oesophagus lined with ciliated 
epithelium have been described. ^ 



The Stomach. 

Malformations. 

Malformations of the stomach are not common. The organ may be entirely want- 
ing in acephalous foetuses. It may be of various degrees of smallness, sometimes no 
larger than the duodenum. It may be divided into two halves by a deep constriction 
in the middle. The pyloric orifice may be stenosed or entirely closed. The stomach 
may be outside of the abdominal cavity from a hernial protrusion through the dia- 
phragm or at some point in the abdominal wall. It is found on the right side, instead 
of the left, when the other viscera are transposed, and the position of the cardiac and 
pyloric orifices is correspondingly inverted. 

Congenital stenosis of the pylorus in infants is of occasional occurrence. It is com- 
monly due to fibrous hyperplasia of the submucosa, sometimes involving the internal 
muscular layers. ^ 

Cadaveric Changes. 

The mucous membrane of the stomach is liable to undergo considerable alterations 
soon after death owing to changes in the distribution and composition of the blood and 
to the action of the digestive fluids. The blood is apt to collect in the small veins, 
especially at the fundus, while by diffusion of the coloring matter, red or brown or 
black streaks and patches form in the mucous membrane. 

Those portions of the mucosa on which the food and digestive fluids collect, usually 
at the fundus and on the posterior aspect of the stomach, frequently appear gray, tur- 
bid, and are soft, and are easily rubbed off. The epithelium in these regions is unusu- 
all}" granular or disintegrated, and is often detached. Sometimes this post-mortem 
softening involves the entire thickness of the stomach wall, which is converted into a 
gray or yellow or brown gelatinous pulp. Thus large or small post-mortem perfora- 
tions may occur. 

INJURIES. 

Perforating wounds of the stomach usually give rise to a fatal perito- 
nitis. It is possible, however, for the wound to heal, or a gastric fistula 
may be formed. 

Eupture of the stomach may be produced by severe blows or falls. 

' For recent bibliography of lesions of oesophagus see Tliorel, Lubarsch and Oster- 
tag's "Ergebnisse," Jahrg. v. for 1898, p. 128. 

- See Meltzer, Xew York Med. Record, August 20th, 1898, bibliography ; also Bol 
lesion and Crofton-Aikins, British Med. Jour., 1900, vol. ii., p. 1768. 



494 THE DIGESTIVE SYSTEM. 



H-aSMORRHAGE. 

Small extravasations of blood in the wall of the stomach are fre- 
quently found in persons who have died from one of the infectious dis- 
eases. 

Haemorrhage into the cavity of the stomach may occur in a variety 
of ways. It may take place from injuries or poisons; from ulcers or 
carcinoma ; from rupture of small aneurisms of the stomach, or from the 
rupture into the stomach of aneurisms elsewhere. It may occur in in- 
fectious diseases, especially in yellow fever, or in diseases of the blood. 
It may be associated with passive congestion of the stomach in hepatic 
cirrhosis of the liver, obstruction of the portal vein, chronic disease of 
the heart and lung ; with an enlarged spleen and in chronic gastritis. In 
the new-born and young infants haemorrhage into the stomach not infre- 
quently occurs without apx3arent lesions which would account for it ; or 
there may be ulcers of the mucous membranes, or cardiac disturbances, 
or infection. While the source of haemorrhage into the stomach is often 
evident, in many cases none can be discovered. Considerable bleeding 
can evidently take place by diapedesis in congested vessels. 

Some cases of chronic gastritis are characterized by general bleeding 
from the mucous membranes of the stomach. 



ATROPHY AND DEGENERATION. 

Atrophy of the stomach occurs in a variety of cachectic conditions, 
in chronic inflammation, and in stenosis of the cardiac orifice. 





>^^o 


^ c y^.^ 




rt. " 


c 




^^ , 


. / 




>^ 


- / 


,/' 


-»«,?'■' 




^ 


& S» 


/ 


k 




-, ' v^ 



\ I 



Fig. 277.— Fatty Degeneration of the Epithelium of the Gastric Tubules in Phosphorus 

Poisoning. 

Albuminous Degeneration of the epithelium may occur in infectious 
diseases and in inflammation of the stomach. 

Fatty Degeneration is often associated with arsenic and phosphorus 
poisoning (Fig. 277), 

Amyloid Degeneration of the small vessels is associated with a similar 
process in other jDarts of the body. 



THE DIGESTIVE SYSTEM. 495 



INFLAMMATION. (Gastritis.) 

Acute Catarrhal Gastritis is usually due to the ingestion of irritating 
decomposing or infectious substances and may accompany general infec- 
tious diseases. 

After death the mucous membrane may be congested and swollen, 
or the congestion may have disappeared. The mucous membrane is 



^i^.^^ 



^ - 




Cr 



5rC s ^^V 






7 .-^ 






P 



Fig. 278.— Acute Catarrhal Gastritis. 



Showing the open ends of two gastric tubules. There is a considerable formation of mucus by the 
epitheUal cells, many of which have the so-called " beaker " form. There is exfoUation of epithelium which, 
with mucus and a few leucocytes and red blood cells, covers the surface of the mucous membrane. 

coated with an increased amount of mucus, especially at the pyloric end 
of the stomach. 

The structural changes in the mucous membrane consist chiefly in 
swelling and albuminous, degeneration, and sometimes exfoliation of the 
eiDithelium with an increase in the jDroduction of mucus by the cylindrical 
cells (Fig. 278), while the intertubular tissue and the submucosa may be 
cedematous and contain a few emigrated leucocytes. The solitary lymph- 
nodules may be enlarged from hyperplasia and hsemorrhagic erosions 
may be present. 

Chronic Gastritis.— This, with the continuance of the exciting condi- 
tions, may follow the acute form. It is often associated with the persis- 
tent use of alcohol, with ulcers and carcinoma, with venous congestion 
from heart lesions, cirrhosis of the liver, obstruction of the portal vein 
or ascending vena cava, or chronic diffuse nephritis. These are doubtless 
predisposing conditions rather than actual excitants of the disease. 



496 -^ THE DIGESTIYE SYSTEM. 

The stomach may be normal in size or small or dilated. Its inner 
surface is usually covered with tenacious mucus. The mucous mem- 
brane may be congested with minute haemorrhages or erosions or it may 
be pale and gray or pigmented from former haemorrhages. It may be 
thickened or thinner than normal. Often, owing to irregular thicken- 
ing, it projects in places in the form of minute granules, or it is irregu- 
larly roughened — etat mamelonne — or there may be distinct polypoid out- 
growths. These alterations are usually most marked in the pyloric 
region. Microscopical examination shows alterations varying in different 
parts of the organ and in different stages of the disease. The surface 
epithelium may be degenerated and exfoliated. The detached epithelium 
may with leucocytes be mingled with the mucus covering the surface. 
The gastric glands may be variously altered. They may be dilated, or 
elongated and tortuous, or hyperplastic' or atrophied ; their epithelium 
may be flattened, degenerated, or detached. The interstitial tissue and 




Fig. 279.— Chronic Gastritis. 

Showing a small portion of the new-formed tissue between the gastric tubules. There are many large 

polyhedral cells in the new tissue. 

the submucosa may be infiltrated with small spheroidal cells or new- 
formed larger polyhedral cells (Fig. 279), and new fibrous tissue may 
form (Fig. 280), thus often greatly thickening the mucous membrane 
and causing atrophy of the glands. The lymph-nodules at the base of 
the glands may be enlarged from hyj^erplasia. On the other hand, the 
mucous membrane may, as contraction takes place in the new-formed in- 
terstitial tissue, undergo great atrophy (Fig. 281), so that it is pale, 
thin, often gray in color, with more or less pigmentation. 

The formation of new fibrous tissue may later involve the muscularis 
also, leading to various distortions of the stomach. 

Croupous Gastritis (Membranous or Diphtheritic Gastritis). — This form 
of gastric inflammation, most common in children, may be associated 
with dii^htheria or with other infectious diseases, but may occur indepen- 
dently. In adults it is usually secondary to typhus fever, pneumonia, 

^ See Gone, Welch Anniversary Contributions to the Science of Medicine, p. 877, 
1900, bibliography. 



THE DIGESTIVE SYSTEM. 



513 



Croupous Colitis. — This form of iuflammation may involve the rectum 
alone, or the entire length of the colon, or only its upper portion. The 
mucous membrane is congested and swollen, and coated with a layer of 
false membrane ; the connective tissue betvreen and beneath the gland 




Fig. 296.— NoDrLAR Colitis -with Ulceratiox. 
Showing necrosis and ulceration of the Ij^mph-nodule with opening into the lumen of the gut. 

tubules is infiltrated with fibrin and pus, and in severe cases the inflam- 
mation involves the muscular and peritoneal coats also. The inflam- 
mation is usually more intense at some places than at others, so that the 
surface of the mucous membrane shows the false membrane in isolated 
patches. Less frequently there is a uniform coating with the false mem- 
brane. In mild cases, as the inflammation subsides, the products of in- 
flammation are absorbed and the wall of the intestine returns to its normal 
condition. In more severe cases the quantity of the inflammatory prod- 
ucts is so great that portions of the wall of the intestine become necrotic. 
This necrosis may involve only the glandular coat, or it may extend 




Fig. 297.— Nodular Colitis. 
Fi'om the intestine of a child showing numerous ulcers involving solitary nodules. (Compare Fig. 288.) 



deeper into the wall of the intestine. The necrosed tissue after a time 
sloughs away, leaving behind ulcers of different sizes and depths. After 
this the ulcers may cicatrize, or their floors and walls may remain in the 
condition of granulation tissue for an indefinite length of time. When 
the latter is the case there is added a chronic inflammation of the wall of 
33 



514 



THE DIGESTIVE SYSTEM. 



the intestine between the nlcers, with changes in the mncons membrane 
and thickening of the connective -tissne and muscular coats. 

Necrotic Colitis. — There is a form of inflammation of the colon in 
which considerable areas of the connective-tissue coat become necrotic, 
leaving the glandular coat undermined and separated from the muscular 
coat. In this way large ulcers with overhanging edges are developed. 
This form of colitis is very fatal. 

There is another very fatal and obscure form of necrotic colitis which 
appears to be septic in character. After death the inner surface of the 




Fig. 298.— Necrotic Colitis. 
Circumscribed congestion and necrosis of the glandular and connective-tissue coats. 

colon is found studded with little blackish areas in which the blood-ves- 
sels are gorged with blood. The glandular and connective-tissue coats 
are infiltrated with pus cells and there is a superficial necrosis (Fig. 298). 
Various forms of micro-organisms have been found in connection 
with suppurative and necrotic lesions of the ileum and colon ; Strepto- 
coccus pyogenes, Staphylococcus pyogenes. Bacillus coli communis, Ba- 
cillus proteus. Bacillus pyogenes, and others. The significance of these 
organisms is not yet clear. ' 

^See Kruse and Pasquale, Zeits. f. Hygiene imd Infkr., Bd. xvi., p. 1, 1894; also 
Cerenville, Tavel, and others, Ann. Suisses des Sc. Med., ser. ii., p. 531, 1895. 

See for consideration of Streptococcus enteritidis in infants, Hirscli, Centralbl. f. 
Bak., Abth. i., Bd. xxii., p. 369, bibliography. 

For a study of intestinal bacteria see Lembke, Arch. f. Hygiene, Bd. xxvi., p. 293, 
1896, bibliography. See also Mace's "Bacteriologie," 1901, p. 1140 et seq. 



THE DIGESTIVE SYSTEM. 



515 



Mucous Colitis (Membranous Colitis). — Uuder a variety of obscure con- 
ditions, probably sometimes inflammatory in character, shreds or sheets 
or even cylindrical casts of the interior of the gut are passed from the 
bowels. These consist of dense mucus often mingled with degenerated 
epithelium. ' 

Chronic Colitis. — In prolonged inflammation of the colon marked 
structural alterations may take place. The glandular coat may be uni- 
formly thickened, or thrown into the form of ]3olypoid tumors, or atro- 
phied, or destroyed by ulcers of various sizes and shapes (Fig. 299). 
Small cysts may form from the retention of mucus in the follicles. The 




Fig. 299.— Chronic Colitis with Extensive Ulceration of the Mucous Membrane. 

In places only a few ragged Islets of mucous membrane are left, the muscularis forming the bottom of the 

ulcers. 

connective -tissue and muscular coats may be thickened or thinned. Ap- 
parently chronic colitis may follow any of the forms of acute colitis. 



The Cecum. 

Catarrhal Inflammation of the csecum is not uncommon. It is usually 
produced hj an habitual accumulation of fseces in this part of the intes- 
tine. The course of the inflammation is usually chronic, but marked by 
acute exacerbations. At first the mucous membrane undergoes the or- 
dinarj^ changes of chronic catarrhal inflammation. To this may succeed 
a slow suppurative inflammation which extends through the wall of the 
intestine and gives rise to ulcers and perforations. 

Through these perforations the faeces may pass into the peritoneal 
cavity, or the perforations are partly closed by adhesions, and abscesses 
are formed, or sinuses into the surrounding soft parts. 

Chronic Hyperplastic Tuberculosis of the Ileo-csecal Region and Other 

Parts of the Intestine. — Attention has recently been called to a peculiar 

form of tuberculous inflammation of the intestine which is characterized 

by the extensive formation of small spheroidal -celled and fibrous tissue, 

especially in the submucosa and often involving the muscular wall and 

the subserous layer. Miliary tubercles, cheesy degeneration, and ulcera- 

^ Numerous observations have been made and a large bibliography has been gath- 
ered on what is called membranous enteritis or colitis, for which the reader may consult 
Butler, New York Medical Journal, December 28th, 1895, or Akerlund, Arch. f. Ver- 
dauungskrankheiten, Bd. i., p. 896, 1896. 



516 THE DIGESTIVE SYSTEM. 

tiou are not usually conspicuous features of the lesion. The ileo-ceecal 
region is most often involved, the rectum less frequently, while the lesion 
is rarely limited to the ileum. Both the large and small intestine ]nay be 
involved together. The new tissue may form a circumscribed annular 
thickening of the wall of the gut, or it may occur as a distinct tumor or 
as polypoid projections of the mucous membrane. The intestine in the 
vicinity of the involved portion may be enclosed in a mass of fibrous fat 
tissue. Owing to the thickening of the wall of the intestine the lumen 
may be much narrowed or nearly comj)letely stenosed. On section of 
the thickened areas, caseous foci may be revealed ; ulcerations may be 
in rare cases absent ; more often they are moderate or extensive. 

The microscopical examination shows that while miliary tubercles and 
cheesy degeneration are commonly to be detected, the new tissue consists 
in the main of collections of small spheroidal cells with more or less 
fibrous stroma and occasionally giant cells and of moderately cellular or 
dense fibrous tissue. The polyhedral cells common in tuberculous inflam- 
mation are not as a rule conspicuous. The new tissue is usually most 
abundant in the submucosa. The mucosa may be similarly thickened, usu- 
olly in iDolypoid form, or unchanged ; it may show simple catarrhal altera- 
tions or may contain miliarj^ tubercles or be ulcerated. The muscular 
coat may be also infiltrated and much thickened by the new-formed cel- 
lular and fibrous tissue and there may be muscular hypertrophy. The 
associated lymph-nodes may be involved. Tubercle bacilli are present 
in the lesions, sometimes in enormous numbers. The process appears to 
be sometimes primary in the intestine ; sometimes it occurs with or fol- 
lows tuberculous lesions of the lungs. Hyperplastic tuberculous lesions 
limited to the caecum have frequently been operated upon under the im- 
pression that the process was cancerous. Lartigau has suggested that 
the peculiarities of this process may be due to infection with an attenu- 
ated form of the tubercle bacillus. 



The Eectum. 

Besides inflammatory change s^imilduY to those already described as oc- 
curring in the colon, we sometimes find a suppurative inflammation of 
the connective tissue which surrounds the rectum, either associated with 
lesions of the mucous membrane or occurring by itself. 

In adults the lower end of the rectum is the part of the intestine 
v/hich is the most frequent seat of syphilitic ulceration. Most of these 
ulcers seem to be the result of unnatural coitus, or of infection from 
specific sores of the vulva ; but some of them seem to be due to the soft- 
ening of gummy tumors. The gonococcus is an occasional excitant of 
inflammation of the rectum. 

Strictures of the rectum may be due to tumors, to cicatrices following 
trauma or inflammation. ' 

^ For bibliography -of non-malignant rectal strictures ^qq Peterson, Jour. Am. Med. 
Assn., vol. xxxiv., p. 259, 1900. 



THE DIGESTIVE SYSTEM. 517 



The Appendix Yehmifoemis. 



Inflammation — Appendicitis. — Inflammatiou of the apiDendix may pre 
sent various phases. 

1. The mucous membrane may be the seat of acute catarrhal inflamma- 
tion. This is of inild type and short duration, with congestion, swelling, 
and an increased i^roduction of mucus ; or it is of severer type, of longer 
duration, and the cavity of the appendix is distended by mucus and 
pus. 

2. The entire thickness of the wall of the appendix may be the seat 
of an acute exudative inflammation. The appendix is very much increased 
in size, sometimes to the size of a man's finger. This increase in size is 
due, not to a dilatation of the cavity of the appendix, but to a thicken- 
ing of its walls. The walls are congested, swollen, infiltrated with fibrin 
and pus, the peritoneal coat is covered with fibrin. There is neither 
necrosis nor perforation. If the appendix is behind the csecum, or if 
adhesions are formed early, there is only a localized peritonitis. If the 
appendix projects freely into the peritoneal cavity and no adhesions are 
formed, a general peritonitis is soon established. 

3. At one or more points in the wall of the appendix there is an exu- 
dative inflammation icith necrosis. In this way small or large portions of 
the wall of the appendix are destroyed, large or small perforations are 
formed, and the contents of the appendix escai)e into the abdominal cav- 
ity. In these cases the appendix usually contains a faecal concretion. 
Such perforations are usually followed by the collection of pus around 
the appendix (Fig. 300). The pus may extend from this abscess-like 
collection in any direction and for long distances, so that collections may 
be found deep in the pelvic cavity, or under the diaphragm, or abscesses 
may form a^t other remote points. 

4. The entire appendix becomes gangrenous within one or two days, 
with the formation of an abscess, or general peritonitis. This is the most 
fatal form of appendicitis. 

5. Inflammation of the appendix may be secondary to catarrhal or 
croupous colitis. 

6. In typlioid fever there may be changes in the wall of the apiDendix 
of a character similar to those in the wall of the small intestine ; that is, 
hyperi)lasia of the lymphoid tissue with necrosis. 

7. There may be a tuberculous inflammation of the appendix, with the 
formation of ulcers. 

As the result of chronic inflammation in the aj)pendix strictures or 
obliteration of its lumen may occur. 

The lumen of the appendix frequently contains concretions of faecal 
material which have often been mistaken for foreign bodies. Foreign 
bodies, such as grape and apple seeds, and various small objects which 
have been swallowed, sometimes, though rarely, find their way into the 



518 



THE DIGESTIVE SYSTEM. 



appendix. ^ Both the fsecal concretions and the foreign bodies may act 
as important jDredisposing agents of inflammation and perforation of the 
appendix, through pressure, erosion, etc., of the mucous membrane, 
affording portals of entry to various forms of pathogenic micro-organisms. 



















VMWm^t 









Fig. 300.— Acute Suppurative Appendicitis. 

Appendix removed by operation twelve hours after first symptoms. Streptococcus was found in the 
exudate. 1, Mucous membrane of the appendix ; 2, lymphatic nodules in the mucous membrane ; 3, sub- 
mucosa ; 4, muscularis ; 5, mesentery of the appendix ; 6, pus and fibrin covering the appendix ; 7, dense 
infiltration of the wall of the appendix with pus. 

The bacteria most commonly found associated with the lesions of acute 
appendicitis and its accompanying peritonitis are Streptococcus pyogenes, 
Staphylococcus pyogenes, the Bacillus coli communis, and Bacillus 
proteus. ^ 



TUMORS OF THE INTESTINE.=^ 

Fibroma and Lipoma may be developed from the submucous coat and 
grow inward, or from the subserous coat and project outward into the 
peritoneal cavity. 

Myoma may originate in the muscular coat and project inward, ob- 
structing the intestine. In the duodenum such tumors may obstruct the 

^ For a study of foreign bodies in appendix see Mitchell, Johns Hopkins Hospital 
Bulletin, vol. x., p. 35, 1899. 

'^ Hodenpyl, "Etiology of Appendicitis," ]^ew York Medical Journal, December 
30tli, 1893. Consult also Kelynack, " Patliolog}'' of the Vermiform Appendix," London, 
1893. Berry, Jour, of Path, and Bact., vol. iii., p. 160, 1895 (bibliography). Ribhert, 
Virch. Arch., Bd. cxxxii., p. 66. For bacterial report see Loic, Reports Boston City 
Hospital, Ser. 11, 1900, p. 173. 

^For a study of congenital tumors of the intestines consult Hueter, Ziegler's Bei- 
trage zur path. Anat., Bd. xix., p. 391, 1896. 



THE DIGESTIVE SYSTEM. 519 

common bile duct. Less frequently these tumors project outward into 
tlie peritoneal cavity. 

Polypoid Growths, i^rojecting into the cavity of the intestine and com- 
posed of connective tissue and covered with epithelium, are frequently 
found. They are associated with catarrhal inflammation or occur by 
themselves. They are found throughout the intestinal tract and may be 
single or multiple. They grow from the submucous coat and project in- 
ward. Some of them are small, solid connective-tissue tumors, covered 
b}" the mucous membrane which they have pushed inward. Others are 
of the same character, but of large size. In others the connective tissue 
is arranged in branching tufts, covered with cylindrical epithelium ; and 
in these last tumors there may also be tubules lined with cylindrical 
epithelium, giving to the growth the characters of an adenoma. 

Lymphoma. — Growths of tissue somewhat resembling that of the lym- 
phatic tissue of the lymph -nodes may originate in the solitary and agmi- 
nated nodules, and in the intestinal wall in cases of leukaemia and pseudo- 
leuksemia (Fig. 301). 

Similar groAvths are found as independent lesions both in the large 
and small intestines. These are irregular, diffuse growths infiltrating 
the wall of the intestine, the mesentery, and the neighboring lymph - 
nodules, and may reach a considerable size. They often ulcerate inter- 
nally and may lead to dilatation or stenosis of the intestine. The classifi- 




Fig. 301.— " Lymphomata " of the Intestine in Pseudo-Leukemia— Hodgkin's "Disease. 

The growths are polypoid, many are pigmented, and they were in this case widely distributed over the in- 
testinal mucosa. 

cation of such tumors is difficult and it is often doubtful whether they 
should be groui^ed with the sarcoma or the so-called lymphoma. 

Sarcomata are of occasional occurrence in the intestine. They appear 
to be more frequent in the small intestine and in the rectum than in the 
large intestine. While various structural types are recorded, the so- 
called lympho- sarcomata are most common.^ 

Adenomata are found in the duodenum and colon. They form flat 

^ For resume and bibliography of sarcoma of small intestine see Lihman, Am. Jour. 
Med. Sciences, vol. cxx., p. 309,' 1900. For a resume with bibliograph}^ of melano- 
sarcoraa of the rectum see Wiener, Ziegler's Beitrage, Bd. xxv., p. 322, 1899. 



520 THE DIGESTIVE SYSTEM. 

infiltrations of the wall of the intestine, or i)roject inward as polypoid 
tumors. They are composed of tubular follicles, like those of the intes- 
tinal mucous membrane, and of a connective -tissue stroma. In some of 
these tumors the tubules have a regular shape and arrangement ; there is 
no infiltration of surrounding tissue ; the tumor is of benign nature. In 

other tumors the tubules are irreg- 
ular in shape and arrangement, 
t >. '^".j ^ . ,. . V ' V ^^^ ^"^^ growth infiltrates the sur- 

J^'' -' '; ' \ ^^~'' '' : "■> y^ rounding parts (Fig. 302 ) . 

'f\C''-l' ^. >>VV' ff^' There is no sharp dividing line 

*' ' ^' ''"'''' '-'.i i between these tumors and the car- 



I. 



[ ! ' ''' { cinomata. 



Fig. 303.— Adenoma of the Rectum. 

as extended through the r 
cosffi into the suhmucosa. 



Carcinoma develops most often 
W . in the colon and the duodenum. 

The forms which have been de- 

' \'i ■, ^ r- '- c'A " scribed in the stomach occur 

// -^^^ , U also here, i.e.: 1. The medullary 

^O ^ ^^S:'.Z _ /orms with relatively little stroma, 

.-'- ' ^^ C.-^Clrs) '-" '^-^ and epithelial cells either in solid 

y. C^j': r- U ^■'^' '^ masses within the alveoli ; or 

maintaining in a measure the 
gland type — -adeno - carcinoma. 

The growth has extended through the muscularis mu- 9 Vihrnu^ farm <ipirr}i^i<i ^ 

^ cosse into the suhmucosa. ^- -^ ^^^^ OllS JO) m — SCtt ) flUS. 6. 

Gelatinous forms, which are more 
common here than in the stomach. Epithelioma often involves the anus 
and rectum. 

Tumors of the Appendix are rare — fibroma, lipoma, myoma, sarcoma, 
endothelioma, and carcinoma are recorded. ' Several cases of primary car- 
cinoma of the appendix have been observed.^ 



INTESTINAL CONCRETIONS. (Enteroliths.) 

There are sometimes found in the intestines round, oval, or irregular 
masses of firm consistence. They are usually small, but may reach the 
size of a man's fist. They are composed of fsecal matter, mucus, bile, 
the carbonate and phosphate of lime, and triple phosphate. They may 
induce inflammations, ulceration, and perforation. 

The animal parasites of the gastro -intestinal canal have been already 
considered in another part of this book.^ 

' For bibliography of tumors of the appendix see Kelly, Proc. Path. Soc. of Phila- 
delphia, n. s., vol. iii., p. 109. 

^WMpJiam, Lancet, 1901, vol. i., p. 319. 

2 For recent bibliography of lesions of the intestines see TJiorel, Lubarsch and Os- 
tertag's " Ergebnisse, " Jahrg. v. for 1898, p. 171. 



THE DIGESTIVE SYSTEM. 521 

The Peritoneum. 

Malformations. 

Arrest in development of the peritoneum may be manifested in fissures in the 
mesial line or external to it; in absence of the diaphragm; in fusion with the pleura; 
and in incomplete formation of the mesentery, the omentum, and the other folds of the 
peritoneum. 

Excess of development occurs in the shape of unusual length of the mesentery, the 
omentum, and the other folds of the peritoneum; or of supernumerary folds and 
pouches. These are chiefly found in the hypogastric, iliac, and inguinal regions and 
near the fundus of the bladder. There may be access to these sacs by a well-defined 
fissui'e or ring, which is frequently surrounded by a tendinous band lying in the dupli- 
cature. These may give rise to internal incarceration of the intestines. 

ASCITES. 

The collection of transudate in the peritoneal cavity may be the re- 
sult of chronic venous congestion, especially in connection with obstruc- 
tion of the portal circulation in cirrhosis from thrombi, emboli, etc., or 
with chronic heart and kidney diseases. It is often associated with 
similar conditions in the pleura and pericardium. Chylous ascites may 
result from a rupture of the thoracic duct or from a transudation from 
the chyle vessels. ' 

INFLAMMATION. (Peritonitis.) 

Acute Peritonitis. — Acute inflammation of the peritoneum may occur 
as a primary process, but is much more often secondary. In the latter 
case it may be associated with wounds and contusions of the wall of the 
abdomen; wounds, ulcers, new growths, incarcerations, intussuscep- 
tions, rui)tures, perforations, and inflammations of the stomach and in- 
testines; inflammation of the vermiform appendix ; injuries, ruptures, 
and inflammations of the uterus, ovaries, and Fallopian tubes ; rupture 
and inflammation of the bladder ; inflammation of and about the kidneys ; 
abscesses and hydatid cysts of the liver ; inflammation of the gall-bladder 
and large bile ducts ; thrombosis of the portal vein ; inflammations of the 
spleen, pancreas, lymphatic glands, retroperitoneal connective tissue, 
vertebrae, ribs, and jDclvic bones ; pysemia and other infectious diseases. 
The inflammation is at first either local or general. A local peritonitis 
may remain circumscribed, or it may spread and become general. 

AYe may distinguish two anatomical forms of acute peritonitis. 

1. Cellular Peeitois^itis. — This form of peritonitis may be in- 
duced by any irritant which does not act too energetically. It can be 
excited in dogs by intraperitoneal injections of very small quantities 
of a solution of chloride of zinc. In the human subject we find it with 

' For a studv of milkv fluids in serous cavities consult Shaw, Jour. Path and Bact., 
vol. vi., p. 339,^1900, bibliography. 



522 THE DIGESTIVE SYSTEM. 

perityphlitis, with circumscribed abscesses in the peritoneal cavity, in 
puerperal fever, and other infectious diseases with early death. 

At the autopsy the entire peritoneum may be congested ; but there 
are no exudates and no other lesions visible to the naked eye. Minute 
examination, howe^ er, shows a very marked change in the mesothelial 
(endothelial) cells. These are increased in size and number, and the 
new cells coat the surface of the peritoneum and project outward in lit- 
tle masses (Fig. 303). This form of inflammation, in many cases at least, 
if life be prolonged, passes into the exudative phase, next to be considered. 



=^^ 







^^ . 



FIG. 303.- ACUTE Cellular Peritonitis— Human Omentum. 

There are swelling and proliferation of the mesothelial cells as well as of the cells of the fibrillar tissue form- 
ing the omental traheculae. 

2. Exudative Perito^sHtis. — This which is the common form of 
acute peritonitis presents lesions similar to those which have been already 
described in pleuritis and pericarditis. Thus there is a form in which 
fibrin is the chief exudate with but little serum ; or the exudate is sero- 
fibrinous, or purulent, or h?emorrhagic. When fibrin is present, the in- 
testinal coils may be more or less firmly adherent to the abdominal walls 
or to each other. If putrefactive bacteria be present, as in peritonitis 
from perforation of the intestine, the exudate may be f ouL 

In local inflammation of the x)eritoneum the position may be indicated 
by the name, thus perihepatitis, perisplenitis, perityphlitis, pelvic, sub- 
phrenic, etc. 



THE DIGESTIVE SYSTEM. 523 

Acute exudative peritonitis may terminate in recovery with absorj^- 
tion of the exudate, permanent connective -tissue adhesions and thicken- 
nings of the peritoneum often remaining. Chronic peritonitis may follow 
the acute phase. 

Bacteria are the usual excitants of acute exudative peritonitis. In 
primary forms of peritonitis the Streptococcus and Staphylococcus pyo- 
genes are the bacteria most frequently present. 

In secondary exudative peritonitis the pyogenic cocci and the colon 
bacillus have been most frequently found. Of the other bacteria which 
have been found in the exudate we may name the pneumococcus, the 
gonococcus/ B. pyocyaneus, B. proteus, B. aerogenes capsulatus, B. 
typhosus. 

There is abundant evidence that bacteria can pass from the intes- 
tinal cavity through its wall into the peritoneum without perforation, 
especially in regions where the integrity of the tissues is impaired by 
disturbances in circulation and nutrition or in necrosis, as in strangula- 
tion of the gut. ^ 

Chronic Peritonitis may follow the acute exudative form or may occur 
independently. The lesions yslyj. In one group of cases the peritoneum 
is beset with minute translucent nodules, sometimes visible, sometimes 
invisible to the naked eye. These are apparently formed by a local pro- 
liferation of the mesothelial and connective-tissue cells. Associated with 
this there may be a general irregular proliferation of the peritoneal meso- 
thelium. This has been called chronic cellular peritonitis. 

In other cases there are local or general fibrous adhesions, sometimes 
firm, sometimes loose, between the intestinal coils or between the intes- 
tine and the abdominal wall. In this way sacculated collections of sero- 
fibrinous or purulent exudate may form in the abdominal cavity. Finally 
chronic peritonitis may result in a dense fibrous thickening of the peri- 
toneum, either local or widespread. 

In some cases the parietal ijeritoneum is x>rincipally involved; in 
others the peritoneum of the stomach, intestines, liver, and spleen. The 
thickening of the capsule of the liver may be attended with a diminution 
in the size of that viscus. There may or may not be adhesions ; serous 
or other exudate may be present. Great distortion of the omentum, 
mesentery, and other abdominal viscera may occur. 

Tuberculous Peritonitis may occur in acute general miliary tuberculosis 
or it may be secondary to tuberculous inflammation elsewhere, as in the 

^ See Cusliing on Gonococcus peritonitis, Johns Hopkins Hospital Bulletin, vol. x., 
p. 75, 1899. 

'^Consult for studies and bibliography of various phases of peritonitis Tai-el and 
Lanz, "Peritonitis," Mitth. a. kl. u. med. Inst. d. Schweiz, 1 Reihe, Heft 1, p. 1, 1893; 
Silberschmidt, ibid., Heft 5, p. 432; Flexner, Philadelphia Med. Jour., November 12th, 
1898; Cullen, Johns Hopkins Hospital Reports, vol. iv., p. 411, 1895; Abramoio, Ziegler's 
Beitr., Bd. xxiii., p. 1, 1898; Buttner, ibid., Bd. xxv., p. 453, 1899. 

For special studies on the entrance of micro-organisms into the bodj^ from the 
gastro-intestinal canal see Opitz, Zeits. f. H3^2:iene, "Bd. xxix., p. 505, 1898; Bircli- 
Hirschfeld. Ziegler's Beitr., Bd. xxiv., p. 304, 18^98; BucTibinder, Deutsche Zeits. f. Chir., 
Bd. Iv., H. 6, and 7, 1900; Marcm, Zeits. f. Heilkunde, Bd. xx., p. 427, 1899; also 
Wiener klin. Wochenschrift, Januarv 3d, 1901. 



524 THE DIGESTIVE SYSTEM. 

lungs or genito -urinary organs or intestines; or it may be an independent 
process. The process may be local or general in the peritoneum. The 
lesions may be miliary in character or there may be large foci of new- 
formed tubercle tissues with considerable necrosis. There may be more 
or less serous or sero -fibrinous or purulent or hsemorrhagic exudate. 
Fibrous adhesions may form between the intestinal coils and the peri- 
toneal walls with the encapsulation of exudate. Ulceration of the 
tubercle tissue may occur, or it may become dense and fibrous and is 
then often pigmented. The tuberculous inflammation may be limited to 
the vicinity of tuberculous ulcers of the intestine. It may involve the^ 
omentum, which is converted into a hard, thick, dense mass at the upper 
part of the abdominal cavity. ' 



TUMORS. 

Fibromata are developed from the subperitoneal connective tissue and 
project inward into the peritoneal cavity. They are found beneath the 
parietal peritoneum and that covering the intestines. Such tumors may 
reach a very considerable size. Papillary fibromata of the peritoneum 
(Fig. 304) may be secondary to papillary fibroma of the ovary. 

Lipomata. — Circumscribed tumors composed of fat tissue are formed 
beneath the intestinal and parietal iDcritoneum and in the mesentery. 
These tumors may become changed into fibrous tissue or calcified. Their 
pedicles may become atrophied so that they are left free in the peritoneal 
cavity. 

When they grow beneath the parietal peritoneum they may form fat 
hernige. At the umbilicus, in the inguinal canal, along the vas deferens, 
in the crural ring, and in the obturator foramen, fatty tumors may grow, 
project outward under the skin like hernige, and, by drawing the peri- 
toneum after them into a pouch, may oi)en the way for a future intestinal 
hernia. 

Very large retroperitoneal and iDcrirenal lipomata are of occasional 
occurrence. ' 

Eetroperitoneal sarcomata are found both in children and adults. 
They usually originate behind the peritoneum, covering the posterior 
part of the abdominal wall, and may grow between the folds of the mes- 
entery. 

They may be of the small spheroidal -celled type (lympho- sarcoma) 
or of the fusiform- celled type. They are often very vascular. At first 
they grow slowly inward, j^ushing forward the peritoneum and abdominal 
viscera. After a time they assume a more noxious character, infiltrating 
the soft parts with which they come in contact, and forming metastatic 

1 For bibliography with reference to operative treatment see Bottomley, Keports 
Boston City Hosp., ser. 11, p. 118, 1900. For a full critical summary of the literature 
of peritonitis from 1885 to 1900 see Biimm, Centralbl. f. Path., Bd. xi'i., pp. 1, 65, 1901. 

2 For bibliography of such tumors see Adami, Montreal Med. Jour., vol. xxv., pp. 
529, 620, 1897. 



THE DIGESTIVE SYSTEM. 



525 



tumors in the omeutum, meseutery, intestinal wall, liver, lungs, and in 
other viscera. ' 

Endotheliomata similar in structure to those originating in the pleura 
are of occasional occurrence in the peritoneum. They may form singie 
Avell- defined tumors or flattened masses in the thickened peritoneum. 
Cuboidal or polyhedral cell masses often grouped along the side of anas- 




FiG. 304.— Papillary Fibroma— Papilloma- of Peritoneum. 

This growth was secondary to a similar tumor originating in the ovary and connected with that or- 
gan (see Fig. 373) . Detached portions of the original tumor were transplanted to various regions of the 
peritoneum. 



tomosing channels in the new-formed or old connective -tissue stroma 
sometimes lend a glandular ax)j)earance to the type of growth. 

These tumors ai)parently originate in the true endothelium of the 
subperitoneal lymph channels and not in the flat cells often called endo- 
thelial — mesothelium — lining the peritoneum. 

Carcinoma of the peritoneum is usually secondary to this disease in 
adjacent regions, stomach, liver, uterus, etc. Its structural characters 
correspond with those of the primary growth. It is apt to appear in 
the form of numerous larger and smaller whitish nodules, sometimes 
local, sometimes widely disseminated over the peritoneal surfaces. Such 
tumors, when small and numerous, may readily be mistaken for tubercles. 

^ See for bibliography Steele, Am. Jour. Med. Science, vol. cxix., p. 311. 



526 THE DIGESTIVE SYSTEM. 

Gelatinous Carcinoma is not infrequent and sometimes seems to be 
primary in the peritoneum. But in such cases the possibility of an origin 
in the mucous membrane of the colon, in which such growths are com- 
mon, and the extension outward without evidence of growth in the gut 
is not improbable. Gelatinous cancer often forms large masses, which 
widely involve the peritoneum and distend the cavity. 

Various forms of tumors of the umbilicus have been described. ' 



CYSTS. 

Cysts of the mesentery are of occasional occurrence.^ They may be 
filled with chyle, with blood, or with serous fluid, or may be due to the 
echinococcus. 

Multiple cysts of the omentum may form by transplantation of papillary 
cyst-adenomata from the ovary (see Fig. 305). 

Dermoid cysts may be found in the peritoneal cavity. Eetroperitoneal 
cysts have been a few times recorded. 

PARASITES. 

Echinococci can be formed in their regular way at any part of the 
visceral and parietal peritoneum, or be free in the peritoneal cavity. 
These cysts may be small, or so large as nearly to fill the abdominal 
cavity. 

Cysticercus cellulosae may also be developed in the subperitoneal con- 
nective tissue. 



The Salivary Glands— The Parotid, Submaxillary, and 

Sublingual. 

INFLAMMATION. 

Acute Parotitis, occurring as an eiDidemic disease known as mumps, 
is usually confined to the parotid gland of one side ; the submaxillary and 
sublingual may be at the same time involved. The gland is swollen and 
there is often oedema of the mucous membrane of the mouth and pharynx. 
Very little is known of the minute changes which the gland undergoes in 
this disease. 

Suppurative Parotitis occasionally occurs as a secondary lesion in a 
variety of diseases, as in typhoid and scarlet fever, pyaemia, pneumonia, 
etc, , and by propagation of inflammation from the mouth. Under these 
conditions the inflammation is usually suppurative and frequently results 
in abscess or sloughing. The interstitial tissue of the gland is more or 
less densely infiltrated with pus cells, and the parenchyma cells may un- 

' See Giannettasio, Arch. gen. de Med., t. iii., p. 52, 1900. 

2 For bibliography of cysts of the mesentery see Bowd, Aunals of Surgery, vol. 
xxxii., p. 461, 1900. 



THE DIGESTIVE SYSTEM. 



527 



dergo fatty degeneration and disintegration. The inflammation may be 
confined to the gland or it may spread to adjacent parts, sometimes 
causing much destruction of tissue, and may give rise to inflammation of 
the brain or of the inner ear, or even to metastatic pysemic abscesses in 




Fig. 305.— Cystic Papilloma of the Omentum. 
Secondary to papilloma of the ovaries. 

different parts of the body. Healing may occur, with the formation of 
salivary fistulse. 

The submaxillary gland may be involved with the parotid in the sup- 
purative inflammation. Acute suppurative inflammation of the connec- 
tive tissue about the submaxillary gland is sometimes of serious imx^ort. 
Sloughing and gangrene may occur and are apt to spread to adjacent 




528 THE DIGESTIVE SYSTEM. 

parts. Septicaemia, oedema of the glottis, or pneumonia may complicate 
the process and cause death. 

The sublingual gland is not often the seat of inflammation. 

Chronic inflammation, leading to the formation of dense interstitial 
tissue, sometimes occurs in the salivary glands. This may occur by 
itself or follow an acute inflammation. Tuberculous inflammation of the 
parotid is not infrequent.^ 

The Excretory Ducts of the salivary glands may become inflamed from 
the presence of foreign bodies or of concretions formed in them. They 
may become occluded from the presence of calculi or as the result of 
inflammation, and may thus become widely dilated both in the main 
branches and in the finer ramifications. The dilatation of Wharton's 

Ml & h^ <''■'') om% 

Fig. 306.— Endothelioma of the Parotid. 

duct to form larger and smaller cysts containing salivary fluid, sometimes 
gives rise to very large and troublesome tumors which constitute one of 
the forms of ranula. ^ . 

TUMORS OF THE SALIVARY GLANDS. 

Fibromata are of occasional occurrence in the parotid. Chondromata, 
endotheliomata, sarcomata and fibro-sarcomata, and myxomata, or more fre- 
quently mixed tumors formed of various combinations of these, are of 
frequent occurrence in the parotid and of occasional occurrence in the 
submaxillary gland. These complex or mixed tumors are of more fre- 
quent occurrence in these glands than in any other part of the body, ex- 
cept possibly the ovary. They are sometimes rendered still more com- 
plicated in structure by the formation of cysts, and what has been 
regarded usually as an atypical glandular growth, lending them an ade- 
nomatous character (Fig. 306). The more recent studies upon the mixed 
tumors of the salivary glands, howevei', ha- '^ led to the belief that a 
large part of these complex growths are endc ta, which are espe- 

1 Consult Meslayand Parent, Gaz. des Hopitaux, February lltli, 1899, bibliography. 

2 For recent bibliography of lesions of t1;e salivary glands see Tliorel, Lubarsch 
and Ostertag's "Ergebnisse," Jalirg. v. for ^-,.3, p. 221. 



THE DIGrESTIYE SYSTEM. 529 

cially prone in thesa regions to undergo secondary degenerative or meta- 
plastic changes/ The parotid endotheliomata differ in many respects 
from those elsewhere in the body and in ways which suggest an origin in 
congenital malformations. 

Fibro-sarcoma and melano-sarcoma have been described. 

A case of rhabdomyoma of the parotid gland, with evidences of atypi- 
cal development of portions of the gland, has been described.^ Primary 
carcinoma of these glands is rare. 



The Pancreas. 

Malformations and Displacements. 

The pancreas may be entn-ely absent in acephalous and double monsters. The 
pancreatic duct may be double; it may open into the duodenum at some distance from 
the biliary duct, or into the stomach. The head of the pancreas may be unduly devel- 
oped and sometimes even completely separated from the rest of the organ, opening 
into the duodenum with a duct of its own. Occasionally there is a small accessory 
pancreas situated beneath the serosa of the duodenum or stomach. 

The pancreas is so firmlj- bound down that its position is not often changed. Some- 
times, however, it is found pressed downward by tight lacing, displaced by aneurisms, 
or contained in umbilical and diaphragmatic hernise. 



ATROPHY, DEGENERATION, AND NECROSIS. 

Atrophy of the pancreas may occur in old age and as a result of press- 
ure from tumors or other adjacent structures. Marked atrophy of the 
pancreas is found in a certain proportion of cases of diabetes mellitus, 
but it is not constant. 

Auto-digestion of x^ortions of the pancreas, intra vitam, has been de- 
scribed, and may, it is believed, lead to localized formation of fibrous 
tissue in the organ. ^ 

Albuminous Degeneration may occur in acute infectious diseases. The 
organ may be red, swollen, and cedematous. The most marked minute 
lesions are swelling and albuminous degeneration of the gland epithelium 
with hyper^emia and interstitial oedema. 

Fatty Degeneration may follow albuminous degeneration and is most 
common in poisoning, especially by iDhosphorus. 

Fatty Infiltration, which should be distinguished from fatty degenera- 
tion, consists in the accumulation of fat in the interstitial tissue of the 
gland. This may be so excessive as to cause nearly entire destruction of 
the gland structures. Under these conditions the outline of the organ 
may be preserved, the fat being enclosed by the capsule. 

Amyloid Degeneration 'lis usually occurs in connection with similar 

^ Volkmann, Deutsche Zt__ f. Chir., Bd. xli., p. 61. 

"^ Pntdden, "Rhabdomyoma of the Parotid Gland," American Journal of the Medi- 
cal Sciences, April, 1883. 

'^Chiari, Prager med. Wochenschrift, v*.! xxv., No. 14, 1900. 
34 



530 



THE DIGESTIVE SYSTEM. 



degeneration in other organs, and is confined to the walls of the blood- 
vessels and the interstitial tissne. 

Hyaline degeneration involving and limited to the islands of Langer- 
hans has recently been described by Opie in a case of diabetes without 
other marked lesions of the pancreas. ' 

Fat Necrosis. — This is a peculiar lesion of the fat tissue, most fre- 
quently seen about the pancreas or between its lobules, but sometimes in 
fat tissue in other parts of the body. White or yellowish nodules, vary- 
ing from the size of a pin's head to that of a pea or larger, are seen em- 
bedded in the fat, the central portion being often soft and grumous. 
They are sometimes calcified and sometimes surrounded by a connective- 




FiG. 307.— Fat Necrosis in the Pancreas. 



tissue capsule. Microscopical examination shows necrosis, degeneration, 
and disintegration of the fat tissue (Fig. 307). 

Fat necrosis is usually associated with lesions of the pancreas — hsem- 
orrhagic infiltration, necrosis, gangrene, and acute and chronic inflamma- 
tory processes. The lesion has been shown to be due to some substance 
in the pancreatic secretion which splits the fat molecule into fatty acids, 
which may crystallize, and soluble substances; calcification is of later 
occurrence. Experimental studies have shown that fat necrosis can be 
induced by such operative procedures as direct the pancreatic secretion 
into fat tissue either immediately about the pancreas or elsewhere.^ 

' Opie, Jour. Exp. Med., vol. v., p. 527, 1901. 

2 For studies in fat necrosis, with bibliography, see Opie, Johns Hopkins Hospital 
Reports, vol. ix., p. 859. 



THE DIGESTIVE SYSTEM. 531 



HiEMORRHAGE. 



Haemorrhage into the substance of the pancreas may occur as the 
result of injury; in the hemorrhagic diathesis; in connection with val- 
vular diseases of the heart or interference with the portal circulation ; or 
in connection with extensive fatty degeneration, or with local necrosis, 
or with fat necrosis of the organ. Such haemorrhages may be minute or 
extensive. Several cases of sudden death are recorded in which the only 
discoverable lesion was an extensive haemorrhage into the substance of 
the gland and the tissue about it. The haemorrhage may be moderate 
and limited to the pancreas, or it may extend into the subperitoneal tis- 
sue for a considerable distance. 

Haemorrhage of the pancreas may be associated with acute inflamma- 
tory changes and with more or less extensive gangrene of the organ. 

INFLAMMATION. (Pancreatitis.) 

Hsemorrhagic Pancreatitis. — In this form of disease haemorrhage simi- 
lar to that above described is associated with suppurative inflammation 
or gangrene or both. The gangrenous pancreas may be more or less en- 
capsulated ; it may be surrounded by pus ; it has by an opening through 
the intestinal wall entered the gut and been discharged. Haemorrhagic 
pancreatitis is often associated with fat necrosis. 

The conditions leading to pancreatic haemorrhage and haemorrhagic 
pancreatitis are not yet fully clear, but recent experimental studies of 
Flexner and Opie indicate that in some cases at least the presence of gas- 
tric juice or of bile or other substances in the pancreatic duct may be of 
great significance. ' 

Suppurative Pancreatitis is not very common, and may be primary or 
due to the extension of a suppurative inflammation from adjacent or dis- 
tant parts of the body. There may be a diffuse infiltration of the organ 
with pus cells or larger and smaller abscesses. The abscesses may open 
into the gastro -intestinal canal or into the peritoneal cavity. The causes 
of primary suppurative pancreatitis are often most obscure. It may be 
associated with fat necrosis and with haemorrhage and gangrene of the 
pancreas. 

Various forms of bacteria have been found in the necrotic, haemor- 
rhagic, and inflammatory lesions of the pancreas, but in most cases the 
significance of their presence is not clear, since necrotic and haemor- 
rhagic foci may afford regions favorable to the lodgment and prolifera- 
tion of micro-organisms which are secondary invaders and whose lesions, 
if such be induced, are comj)licating and not i3riniary . ^ 

^ For a study of the relationships between cliolelithiasis and diseases of the pan- 
creas see Opie, Amer. Jour. Med. Sci., vol. cxxi., p. 27, 1901. 

For a study of experimental pancreatitis see Flexner, University Medical Maga 
zine, vol. xiii., p. 780, 1901. 

- For a detailed consideration of acute inflammation, haemorrhage, gangrene, and 
fat necrosis of the pancreas, with bibliography, consult Fitz, Middieton Goldsmith lee- 



532 THE DIGESTIVE SYSTEM. 

Chronic Interstitial Pancreatitis. — This lesion consists in an increase of 
interstitial connective tissne, which may be general or confined to some 
particular portion of the gland. The new-formed tissue may be interlob- 
ular or interacinar in distribution. ' 

The organ is sometimes enlarged, sometimes smaller than normal. It 
is usually dense and hard ; secondary atrophy of the parenchyma regu- 
larly occurs. It may be associated with chronic inflammatory processes 
in the vicinity of the organ, and obstruction of the pancreatic duct. 

Tuberculous Inflammation. — Larger and smaller tubercles and tubercu- 
lous cheesy nodules are occasionally found in the pancreas in connection 
with acute general miliary tuberculosis or with tuberculous inflammation 
in some other organ, ]3articularly with that of adjacent lymph-nodes, the 
lungs, and the intestine. 

Syphilitic Inflammation. — Chronic interstitial pancreatitis is frequently 
found in congenital syphilis of the new-born, and the gross and micro- 
scopical lesions are similar to those above described. It is not definitely 
established whether or not a similar lesion may be caused by acquired 
syphilis. Gummata are very rare in the pancreas, but have been de- 
scribed in congenital syphilis in very young children. 



TUMORS. 

Carcinoma is the most common and important of the tumors of the 
pancreas. It may be primary or secondary. Primary carcinomata are 
most frequently found in the head of the organ, but may occur in other 
parts. ^ The hard or scirrhous form is most common, but occasionally 
soft and succulent and gelatinous forms are found. They are liable to 
involve adjacent parts by continuous growth, and may form metastases 
in the liver, adjacent lymph-nodes, etc. Secondary carcinoma in the 
pancreas may occur in carcinoma of the stomach, duodenum, and of the 
gall ducts and gall bladder. As a result of carcinoma of the pancreas, 
aside from the extension of the growth, there may be pressure on the 
ductus choledochus, with jaundice; or on the pancreatic duct, with 
cystic dilatation ; or pressure on the duodenum, with stenosis of the gut ; 
or pressure on the vena cava, or portal vein, or superior mesenteric vein, 
etc. , with disturbances of the circulation. 

Cysts. — These are mostly due to dilatation of the pancreatic ducts. 

1. The entire duct may undergo a uniform cylindrical dilatation. 

ture on "Acute Pancreatitis," Trans. New York Path. Soc, 1889. For later bibliog- 
raphy see Warthin, Philadelphia Medical Journal, November 19th, 1898. 

For a brief summary of recorded cases of pancreatic haemorrhage see Anders, Jour- 
nal American Med. Assn., 1899, vol. ii., p. 1391. 

See for critical review of studies on diseases of the pancreas in general, Klippel and 
Lefas, Arch. gen. de Med., t. ii., p. 74, 1899, bibliography. 

' For details of the lesions in chronic pancreatitis, with a study of changes in the 
islands of Langerhans, consult Opie, Journal Experimental Medicine, vol. v., p. 397, 
1901, bibliography; see also ibid., p. 527. 

^ For recent bibliography of primary carcinoma of the pancreas see Baldwin, Phila- 
delphia Med. Journal, December 22d, 1900, bibhography. 



THE DIGrESTIYE SYSTEM. 533 

With this cylindrical dilatation we sometimes find associated small sac- 
cnli. 

2. There may be sacculated dilatations at some points in the ducts. 
These dilatations form cysts of large size, as large even as a child's head. 
Their walls frequently undergo degenoration and calcification. These 
cysts often become filled with blood, and may then be mistaken for 
aneurisms. 

3. The small branches of the pancreatic duct may be dilated so as to 
form a number of small cysts. These cysts are filled with serum, mucus, 
pus, or a thick, cheesy material. 

C3^sts of the pancreas may result from trauiua, inflammatory closure 
or obstruction of the ducts, from old areas of necrosis or haemorrhage, 
and in other ways. ^ 

Concretions of carbonate and phosphate of lime are frequently found 
in the pancreatic ducts. They are usually multiple, small, whitish, 
smooth, or of rough and irregular shapCo Sometimes, however, they 
reach a diameter of more than an inch. They consist chiefly of calcium 
phosphate and carbonate. Besides these free concretions the walls of 
the ducts are sometimes encrusted with salts of lime. Such concretions 
may produce dilatation of the pancreatic ducts and large cysts, or more 
rarely abscesses. 

Foreign Bodies. — Gall stones sometimes find their way into the pancre- 
atic duct. Ascarides have been found in the ducts in a considerable 
number of cases. 

^ Consult Tilger, " Cysts of Pancreas," Virch. Arch., Bel. cxxxvii., 348, bibliography; 
also Fitz, Trans. Assn. Am. Phys., vol. xv., p. 254, 1900. 



CHAPTER VIII. 

THE LIVER. 

Malformations. 

Congenital malformations of the liver are not common and are of little practical im- 
portance. The organ may be entirely wanting ; the lobes may be diminished or in- 
creased in number; its form may be altered, so that it is rounded, flattened, triangular, 
or quadrangular. The gall bladder or gall ducts may be wanting; the ductus choled- 
ochus may be double, both ducts emptying into the duodenum, or one emptying into 
the duodenum, the other into the stomach. The single ductus choledochus may also 
empty into the stomach. Owing to abnormal openings in the diaphragm or the abdomi- 
nal parietes, the liver may suffer displacement upward or forward. In congenital 
transposition of the viscera the liver is found on the left side, the stomach and spleen 
on the right side. 

Small, isolated bodies, having the same structure as the liver, have been a few times 
found in the suspensory ligament and in the lesser omentum. 



Acquired Changes in Size and Position. 

As a result of tight lacing very marked changes are sometimes produced in the 
shape of the liver. By the narrowing of the base of the thorax the organ is compressed 
from side to side, and its convex surface is pressed against the ribs. In consequence 
of this there are found ridges and furrows on its convex surface. In consequence also 
of the circular constriction, a part of the right, and usually of the left lobe also, be- 
comes separated by a depression. Over this depressed and thinned portion of the liver 
the capsule is thick and opaque. In extreme cases the depression and thinning reach 
such an extent that there is only a loose, ligamentous connection between the separated 
portion and the liver. 

A series of depressions are sometimes found on the upper surface of the right lobe 
of the liver, running from front to back, apparently caused by folds of the organ. 

Structural alterations in the liver may induce changes in its size and shape. It 
may be increased in size by tumors, hydatid cysts, abscesses, fatty and amyloid degen- 
eration, by congestion, and sometimes by cirrhosis, etc. 

It may be diminished in size by atrophy, by cirrhosis, by acute parenchymatous 
degeneration, etc. 

Changes in the position of the liver are produced by alterations in its size, by press- 
ure downward from the thoracic cavity and upward from the abdomen, by the con- 
striction of tight lacing, by tumors or circumscribed serous exudation between the liver 
and diaphragm, by curvature of the spine. 

The liver is readil}^ turned, by pressure from above or below, on its transverse axis. 
The transverse colon may be fixed above the liver so as to push it backward, downward, 
and to the right. There are a few cases recorded of dislocated and movable livers. 
These occurred in women who had borne children and whose abdominal walls were lax. 
With ascites it is not uncommon to find the liver quite movable.' 

'See Graham, "Displacements of the Liver," Trans. Assn. Am. Pliys., vol. x., p. 
258, 1895, bibliography. 



THE LIVEE. 535 



WOUNDS, RUPTURE, AND HAEMORRHAGE. 

Wounds of the liver may induce hajmorrhage, which, if life continue, 
is followed by inflammation. Serious wounds of the liver are usually 
fatal, but recovery may occur even after the destruction of a consider- 
able portion of the oi-gan. 

Rupture of the liver may be produced by severe direct contusions or 
by falls. It may be jDroduced in children by artificial delivery. The 
rupture usually involves both the capsule and a more or less consider- 
able i)ortion of the liver tissue. It is commonly accomj^anied by large 
haemorrhage, and is usually fatal. 

Haemorrhage. — Extravasations of blood in the substance of the liver, 
or more frequently beneath the capsule, may be found in new-born chil- 
dren after tedious or forcible labors. In adults, hsemorrhage, except as 
the result of injury, is uncommon. Extravasations of blood are some- 
times seen in malignant malarial fevers, especially in tropical climates ; 
in scurvy, purpura, and phosphorus poisoning ; and bleeding may occur 
in and about soft tumors, abscesses, and echinococcus cysts. It may 
also occur as a result of thrombosis of the hepatic vein. 

AN-ffiMIA AND HYPERiEMIA. 

Anaemia of the liver may be general or partial. It may be due to 
general anaemia or to local disturbances of the circulation, such as swell- 
ing of the cells in parenchymatous or other degeneration, pressure of 
tumors, etc. The organ appears pale, often of slightly yellowish or 
brownish color. It may be harder than usual, and smaller. 

Hyperaemia of the liver is either an active or a passive process. In 
health the amount of blood in the liver varies at different times, being 
regularly increased during the processs of digestion. When the diges- 
tive process is unduly influenced by the ingestion of spirits, sj^ices, etc. , 
the hyperaemia assumes abnormal proportions, and when this is often 
repeated it may lead to structural changes in the organ. Severe contu- 
sions over the region of the liver sometimes cause a hyperaemia, which 
may result in supj^urative or in productive inflammation. In hot cli- 
mates and in malarious districts active and chronic hyperaemia of the 
liver are frequent and often incite structural lesions. In scurvy, also, 
the liver is sometimes congested. Cessation and suppression cf the 
menses and of haemorrhoidal bleeding may be followed by hyperaemia of 
the liver. In all these varieties of active congestion the liver is enlarged, 
of a deep red color, and blood flows freely from its cut surface. 

Passive congestion of the liver is produced by an obstruction to the 
current of blood in the hepatic veins. Valvular diseases of the heart, 
emphysema and fibrous induration of the lungs, large pleuritic effusions, 
intrathoracic tumors, angular curvature of the spine, aortic aneurisms 
pressing on the vena cava, and constrictions of the vena cava and of the 



536 THE LITER. 

hepatic veins, may all lead to a chronic hypersemia of the liver. In such 
cases, since the congestion affects principally the hepatic veins, we find 



■r^' 



^S - m 



Fig. 308.— Chronic Coxgestiox of the Liter— ''Nutmeg Liver." 

The liver cells are completely atrophied except in the peripheries of the lohules. The central portions 
of the lobules which in the fresh organ are darker than the periphery are lighter in the preserved specimen 
from which this section was cut because the haemoglobin has been dissolved out of the red blood cells. 

the centre of each acinus congested and red while its periphery is lighter 
in color. This gives to the liver a mottled or nutmeg appearance (^nut- 
meg liver) (Fig. 308). The liver cells in the centre of each acinus are 
frequently colored by little granules of red or black pigment, and the 



V 



Fig. 309.— Chroxic Coxgestiox of the Liter. 

Showing a single lobule. The capillaries about the central vein are widely distended with blood— de- 
colorized ; the liver cells on the borders nearest the dilated capillaries show various phases of pressure 
atrophy. 



THE LITER. 537 

cells at the periplierj^ become fatty, so that the nutmeg appearance is still 
more pronounced. A liver in this condition is usually of medium size, 
but may be smaller or larger than normal. 

When the congestion is long-continued the veins at the centre of each 
acinus may become permanently dilated, and the hepatic cells in their 
meshes become atrophied (Fig. 309), so that the centre of each acinus 
consists only of dilated capillaries or of these and new connective tissue ; 
or the dilatation and atrophy of the liver cells may, in circumscribed 
portions of the organ, involve the entire acinus. In long- continued 
congestion the liver is usually smaller than normal, and may be slightly 
roughened or uneven on the surface ; but it is sometimes enlarged. The 
peculiar nutmeg appearance may be very well marked, or it may not be 
evident, the organ being of a dark-red color. 



LESIONS OF THE HEPATIC VESSELS. 

The Hepatic Artery. 

The hepatic artery is in rare cases the seat of aneurisms which may 
attain a large size. Such aneurisms may displace the liver tissue, com- 
press the bile ducts so as to cause jaundice, and may rupture into the 
stomach or abdomen. 

Owing to its abundant anastomoses, emboli of the branches of the 
hepatic artery usually induce no marked lesions, but they sometimes 
result in haemorrhagic infarctions. 

The Portal Vein. 

Thrombosis, Embolism, and Inflammation. — Thrombosis of the branches 
of the portal vein may be produced by weakening of the circulation from 
general debility' — marasmatic thrombi; by pressure on the vessel from 
without, as in cirrhosis, tumors, gall stones, dilatation of the bile ducts, 
etc. ; by injury; by the presence of foreign materials within the vessel; 
and as a result of inflammation of its wall, or of embolus. The throm- 
bus may form in the vessels in the liver or be propagated into them from 
without. It may x)artially or entirely occlude them. The clot may be- 
come organized as a result of endophlebitis, and a permanent occlusion 
of the vessel ensue. If the clot be a simi^le, non -irritating one, leading 
to occlusion, the consequences are usually more marked in the abdomi- 
nal viscera than in the liver itself. The branches of the hepatic artery 
form sufficient anastomoses to nourish the liver tissue and prevent its 
necrosis, even in comj)lete occlusion of the portal vein ; and if occlusion 
occur slowly the organ may continue to perform its functions. But this 
obliterative form of thrombosis is usually attended by ascites, enlarge- 
ment of the spleen, dilatation of the abdominal veins, and sometimes by 
haemorrhage from the stomach and intestines. 



538 THE LIVEK. 

In another class of cases, in addition to the local and mechanical 
effects of a thrombns, the latter may be infections, then there are ne- 
crotic changes and snpjDnrative inilammation in the walls of the ves- 
sels or in the liver tissne abont them. The thrombi are apt to soften and 
break down, and the fragments may be disseminated throngh the smaller 
trnnks of the portal vein. In this way, by the distribntion through the 
smaller vessels of a disintegrated thrombns from a large trunk, or by the 
introduction into the branches of the portal vein of purulent or septic 
material from some of the abdominal viscera or from wounds, multiple 
foci of purulent inflammation in the portal vein, and multiple abscesses 
involving the liver tissue, may be produced. In many cases the pres- 
ence of bacteria may be detected in the inflammatory foci. 

These soft thrombi of the portal vein and the accompanying pyle- 
phlebitis and abscess are induced in a variety of ways. Ulceration of 
the intestines and stomach, abscesses of the spleen, suppurative inflam- 
mation of the mesentery and mesenteric gla^nds, inflammation and ulcer- 
ation of the bile ducts from gall stones, inflammation of the umbilical 
vein in infants, may all induce thrombi in their respective veins, which 
may be projDagated to the portal vein or may give rise to purulent or 
septic emboli. Two cases are recorded in which a flsh bone in the por- 
tal vein induced supiDurative inflammation in that vessel. 

Infarction of the liver after embolism is rare owing to the anastomosis 
between the branches of the hepatic artery and the capillaries of the lob- 
ules. Occasionally atrophy of the parenchyma in circumscribed areas 
follows thrombosis or embolism of branches of the portal vein. 

In infants inflammation of the umbilical vein may not only induce 
inflammation of the portal vein and abscesses in the liver, but multiple 
abscesses in various parts of the body, and acute peritonitis may follow. 

Rupture of the Portal Vein, with fatty degeneration of its walls, has 
occurred in a few instances. 

Chronic Endophlebitis, with atheroma and calcification, may occur in 
the walls of the portal vein, giving rise to thrombosis. 

Dilatation of the Portal Vein, either uniform or varicose, may occur in 
various parts of the vessel or its branches. It may be caused by destruc- 
tion of the liver capillaries in cirrhosis, or by occlusion of the vein by 
thrombi, tumors, etc. 

The Hepatic Veins. 

The hepatic veins present lesions similar to those of the portal vein and 
its branches, but they are much less frequent. The veins may be dilated 
by obstruction to the passage of venous blood into the heart. They may 
be the seat of acute and chronic inflammation, and soft thrombi and sup- 
purative inflammation may be produced by abscesses in the liver. Earely 
there is a localized obliterating phlebitis in the hepatic vein followed by 
chronic congestion, interstitial inflammation, and thrombosis. ' 

' Consult for obliterating phlebitis of the main trunks of the hepatic vein as a cause 
of death, Ghiari, Ziegler's Beitr., Bd. xxvi., p. 1, 1899, bibliography. 



THE LIVER. 539 



ATROPHY. 



Atrophy of the liver may affect the entire organ or be confined to 
some part of it. General atrophy may occur in old age as a. senile 
change, or may be induced by starvation or chronic exhausting diseases. 
The organ is diminished in size, is usually firm, and the acini appear 
smaller than usual. Microscopically the change is seen to be due to a 
diminution in size of the liver cells, and hand-in-hand with this there 
occurs frequently an accumulation of pigment granules within the atro- 
phied cells. The cells may entirely disappear over circumscribed areas, 
leaving only shrivelled blood-vessels and connective tissue ; or, in some 
cases, there may be an increase of connective tissue in connection with 
the atrophy of the cells. When much pigment is formed in the cells the 
lesion is often called pigment atrophy. 

Essentially the same changes may occur in circumscribed portions of 
the liver, as the result of pressure from new connective tissue in cirrhosis, 
from tumors, hydatids, amyloid degeneration, gall stones, etc. In at- 
rophy from pressure the liver cells are apt to become very much flat- 
tened and squeezed together as they diminish in size. 

DEGENERATION. 

Albuminous Degeneration. — In the infectious diseases and in certain 
cases of acute anaemia and phosphorus poisoning — the liver is swollen 
and, on section, of a dull yellowish-gray color, looking as if it had been 
boiled. It contains less blood than usual, and the outlines of the lobules 
are indistinct. Microscopical examination shows the lesion to consist of 
a swelling of the liver cells and an accumulation in them of moderately 
retractile, finer and coarser albuminous granules. These granules may 
disapx^ear and the cells return to their normal condition, or fatty degen- 
eration may follow. Fatty and parenchymatous degenerations are often 
associated. 

Focal necrosis of liver cells occurs in many acute infectious diseases 
(see page 178). 

Acute Parenchymatous Degeneration (Acute Yellow Atrophy) . — This rare 
disease is characterized anatomically by a rapid diminution in the size 
of the liver as the result of a granular and fatty degeneration and disin- 
tegration of the liver cells. The liver, sometimes within a few days, 
may be reduced to one-half its normal size. On opening the abdominal 
cavity the organ may be found lying, concealed by the diaphragm, close 
against the vertebral column. The amount of diminution and the gen- 
eral appearance of the affected organ dei^end to a considerable extent 
uiDon its previous condition — i. e. , whether or not it was the seat of other 
lesions — as well as upon the degree of degenerative change. In general, 
if the lesion is well marked, the liver is small, flabby — sometimes almost 
fluctuating — and the capsule wrinkled. On section the cut surface may 



540 



THE LITER. 




FIG. 310. 



-Fattt Infiltration of Liter 

Cells. 



sIlow but little trace of lobular structure, but presents an irregular mot- 
tling with gray, oclire -yellow, or red ; sometimes one, sometimes another 
color preponderating. 

Microscopical examination shows varying degrees of degeneration and 
destruction of the liver cells. Most evidently in those parts which have 
a grayish appearance, the outlines of the cells are preserved and the 
protoplasm is iilled with larger and smaller granules. In the yellow por- 
tions the outlines of the liver cells may 
be preserved, and they may contain 
varying quantities of larger and smaller 
fat droplets and granules of yellow 
pigment. Or the cells may be com- 
pletely disintegrated, and in their place 
are irregular collections of fat droplets, 
pigment granules, red and yelloAv crys- 
tals, and detritus ; only the connective 
tissue and blood-vessels of the original 
liver tissue remaining. The red areas 
may show nearly complete absence of 
liver cells and cell detritus, and sometimes irregular rows of cells which 
are variously interpreted as being new-formed gall ducts or proliferated 
liver cells. In these areas it appears to be, in part at least, the blood 
contained in the vessels which imparts the red color. Sometimes the in- 
terstitial tissue is infiltrated with small spheroidal cells resembling leuco- 
cytes. Crystals of leucin and tyrosin are sometimes found intermingled 
with the cell detritus. In some cases the liver is not diminished in size. 
These lesions of the liver are frequently associated with enlargement 
of the spleen and parenchymatous degeneration of the kidney and of the 
heart muscle. Multiple haemorrhages may occur in the gastro -intestinal 
canal, kidneys, bladder, and lungs. There is usually marked jaundice. 
This disease is more common in women than in men and in many cases 
has occurred in the puerperal state. Eod-shaped bacteria and micrococci 
have been found in the liver, but their significance is doubtful. The 
excitant of the disease is unknown, and it is an open question whether 
it is a disease primarily of the liver or an acute infectious disease with 
local lesions. It is not unlikely that more than one form of lesion is 
grouped under this heading. ' 

Fatty Infiltration. — In the normal human liver there is usually a cer- 
tain amount of fat in the liver cells, and this amount varies considerably 
Tinder different conditions. 

The gross aj^pearance of pathological fatty livers varies a good deal, 
deiDcnding upon the amount and distribution of fat and its association 
with other changes. If the lesion is uncomiDlicated and considerable the 
organ is increased in size, the edges are rounded, the consistence is firm, 
the color yellowish, and the cut surface greasy. The lobules are en- 

^ For more important bibliography of acute yellow atrophy, see Ziegler's " Lehrbuch 
der Pathologie," Bd. ii. 



THE LITER. 541 

larged and their outlines usually indistinct, and the blood content is di- 
minished. The liver is increased in weight. The lesion may be uniform 
throughout the organ or it may occur in ]3atches. In the latter case the 
liver has a mottled appearance, irregular yellowish patches alternating 
with the brownish -red, unaffected portions. 

Fatty intiltration is often associated with chronic congestion {nutmeg 
liver), with cirrhosis and amyloid degeneration; the picture may then 
present considerable complexity. Fatty livers may be stained brown or 
greenish with bile pigment. 

Microscopically the liver cells are seen to contain larger and smaller 
droplets of fat (Fig. 310), and frequently large drops of fat occupy nearly 
the entire volume of the cell, so that the protoplasm may be visible only 
as a narrow, nucleated crescent at one side, or it may disappear alto- 
gether (Fig. 311). 

Fatty infiltration of the liver may occur as a result of excessive in- 
gestion of oleaginous food ; in chronic alcohol, phosphorus, and arsenic 
poisoning ; in certain exhausting diseases accompanied by malnutrition. 



-,o 



A f.:^" 













s( k ^^.r ^ 



^ - ' lf.v\ 






^o«doc-i:^ t:t>:c 'P^'^^a 






Fig. 311.— Fatty Ixfiltratiox of Liter. 



Portion of the periphery of a lobule, showing many Uver cells distended with a single large drop of fat, 
while between these are liver cells with small fat droplets and others flattened by pressure. In this sec- 
tion, hardened by alcohol, the fat has been dissolved, leaving clear spaces. 

as in pulmonary jDhthisis, chronic dysentery, etc. ; and under a variety 
of conditions which we do not understand. It is common in children 
especially in acute infectious diseases. ' 

Fatty Degeneration. — In this condition, which In many cases cannot 
^e^morx)hologically distinguished from fatty infiltration, the fat is be- 
lieved to be formed by a transformation of the protoplasm of the liver 
cells. The fat droplets are, for the most part, very small and abundant, 
though this is not constant. Fatty degeneration of the liver cells fre- 
quently follows, and is associated with, cloudy swelling under the vary- 

^ See Freeman, Archives of Pediatrics, vol. xvii., p. 81, 1900. 



542 THE LITER. 

ing conditions in which this occurs, or it may appear in profound angemia 
and in acute phosphorus and arsenic poisoning. 

Amyloid Degeneration. — In the liver amyloid degeneration may be 
general or local ; so extensive as to give the organ very characteristic 
appearances, or so slight as to be unrecognizable without the aid of the 
microscope. It may be associated with other lesions. When the change 




: - - -' ., \ 

Fig. 31™'.— Amyloid Degeneration of Liver Capillaries. 

The capillaries are much enlarged and occluded by the amyloid material ; the liver cells between them are 

atrophied. 

is extensive and general the liver is enlarged sometimes to more than 
twice its normal size ; the edges are thickened and rounded ; the surface 
is smooth ; the tissue tough, firm, inelastic, more or less translucent, and 
of a brownish-yellow color. The lobular structure may be more or less 
indistinct, or it may become very evident by an associated fatty degen- 
eration of the peripheral or central cells of the lobules. The translu- 
cency and peculiar appearance of the tissue may be best seen by slicing 
off a thin section and holding it up to the light. When the lesion is less 
considerable the liver may be of the usual size, and may feel harder than 
normal, and here and there a translucent mottling may be evident, or 
the degeneration may be apparent only on the addition of staining 
agents. When, as is frequently the case, it is associated with cirrhosis, 
the liver may be small and nodular, and the appearance of the cut sur- 
face varies, depending upon the character of the cirrhotic change and 
the presence or absence of fat. 

This degeneration usually commences in the walls of the intralobular 
blood-vessels, causing them to become thickened and translucent (Fig. 
312). Their lumen may be nearly or entirely occluded. The liver cells 
may be squeezed by the thickening of the vessels and may become par- 
tially or completely atrophied, or they may be fatty. Amyloid degener- 
ation may also involve the interlobular vessels, and in advanced stages 
lai'ger and smaller areas of liver tissue may be almost completely con- 
verted into the dense, refractile substance in which here and there flat- 
tened liver cells may be seen. 



THE LIYEE. 543 

Amyloid degeneration of the liver is nsually associated with a simi- 
lar lesion of other organs. 

Glycogen Degeneration.— This may occur in the liver cells in diabetes, 

PIGMENTATION OF THE LIVER. 

As a result of severe malarial poisoning a ^^ariable amount of brown, 
black, or reddish pigment is often found in the blood. This is usually 
mostly taken u^) by the leucocytes and deposited in various parts of the 
body, chiefly in the liA'er, sixteen, and marrow of the bones. In the liver 
it is usually found enclosed in variously shaped cells which lie especially 
in the blood-vessels (see Fig. 313), but sometimes in the tissue between 
them. The liver cells frequently contain bile pigment, but usually are 
free from the melanotic x)igment characteristic of this malarial condition. 
As the result of this accumulation of pigment the liver may have a dark 
reddish-brown, an olive-brown, or black color (sometimes called bronze 
liver). Pigmentation of the liver may be marked in hsemochromatosis 
(see p. 88). 

Pigment similar in character to that which occurs in the lungs from 
the inhalation of coal dust may be found in the connective tissue along 






^k 






^ '^j 



^^ 






¥iG. 313.— Malarial Pigmentation of the Liter. 

The piprment is largely in the exfoliated endothelium within the capillaries. Pigmented malarial parasites 

may be seen in some of the cells. 

the portal vessels. Inhaled pigment particles may j)ass the lungs and 
bronchial lymph-nodes, and be deposited in the liver as it is in the spleen 
and hepatic lymph-nodes. 

Pigmentation of the liver cells, which is to a certain extent normal, 
may be greatly increased as a result of atrophy, of localized haemorrhage, 
and of obstructiA'e jaandice. 



544 THE LIVEK. 



CALCIFICATION. 

This lesion of the liver is rare. The deposit of lime may be iu the 
vicinity of the arteries or the veins. ^ 



INFLAMMATION. (Hepatitis.) 

Acute Exudative Hepatitis (Purulent Hepatitis). — Purulent or suppura- 
tive inflammation of the liver may be the result of injury; it may be 
secondary to inflammation of the gall ducts or the branches of the portal 
vein. It may occur as the result of the presence of tumors and parasites, 
or from propagation of an inflammatory process from without, as in ulcer 
of the stomach with adhesions to the liver and secondary involvement of 
the latter. It is often directly due to the introduction of bacteria into 
the organ, through the blood-vessels or gall ducts or otherwise. Puru- 
lent inflammation in the liver almost always results in abscess. 

Large atscesses of the liver may be traumatic, but are often due to 
unknown causes. They are not infrequently associated with dysentery, 
and may then be due to the conveyance of micro-organisms through the 
veins, or lymph channels, or peritoneum, or gall ducts from the intestinal 
ulcers. Such abscesses may be due to the presence of the amoeba coli. 
They occur most frequently in tropical climates whence the w^amj^ tropical 
abscess — but are not very uncommon in the temperate zone. They are 
usually single, but there may be several of them. They are sometimes 
so large as to occupy a large part of the lobe. They are most frequent 
in the right lobe, but may occur in any part of the organ. They tend to 
enlarge, and as they do so they approach the surface of the liver. Here 
the contents of the abscess may be discharged into the peritoneal cavity. 
More frequently, however, as they approach the surface, a localized 
adhesive peritonitis ensues, so that the liver becomes bound to adjacent 
parts, and thus the abscess may open into the pleural cavity, or, owing 
to a secondary pleurisy with adhesions, into the lung tissue. They may 
open into the pericardium. They may open externally through the ab- 
dominal wall ; into the stomach, duodenum, colon, or pelvis of the right 
kidney ; into the hepatic veins, portal vein, vena cava, or gall bladder 
or gall ducts. 

The early stages in the formation of large abscesses of the liver are 
but little known. It is probable, however, that in many cases they are 
the result of the confluence of smaller abscesses (Fig. 324). Their con- 
tents, usually bad-smelling, may be thick and yellow like ordinary pus, 
but more commonly they are thin, reddish-brown, or greenish in color 
from admixture with the pus of blood, gall pigment, and broken-down 
liver tissue. Microscopical examination shows the contents to consist of 
fluid with pus cells, more or less degenerated blood, degenerated liver 

^ See Brill and Lihman, Jour. Exp. Med., vol. iv., p. 541, 



THE LIVER. 



545 



cells, fragments of blood-vessels, and pigment granules and crystals. 
The walls of the abscess are usually ragged, shreds of necrotic liver tissue 
hanging from the sides. Microscopical examination of the liver tissue 
near the abscess shows infiltration with pus, flattening of the liver cells 
from pressure, cloudy swelling, and necrosis of those lying along the 
cavity. ' 

The amoebic abscesses are usually free from bacteria. Other ab- 
scesses may contain the Bacillus coli communis, or the Streptococcus 
pyogenes or Staphylococcus pyogenes. 

irot infrequently, however, especially in old abscesses, examination 











Fig. 314 —Small Abscesses in the Liver containing Bacilu. 



both morphological and cultural fails to reveal the presence of micro- 
organisms. 

After the discharge of the contents of the abscess or without this, if 
it be not very large, granulation tissue may form in the wall of the cav- 
ity and a fibrous capsule be produced, enclosing the contents, which be- 
come thickened and often calcareous, and in this condition may remain 
for a long time. Or the connective -tissue walls may approach one an- 
other and join, forming a fibrous cicatrix at the seat of the abscess. 

Small multiple metastatic abscesses are not infrequent in pyaemia. In 
these abscesses we can readily study the various stages of formation. 
Suppurative processes in any part of the body — in the head, upper and 
lower extremities, etc. — may act as distributing centres for micro-organ- 



' Soe Iv a study of tropical abscess of the liver Howard 
led. Sciences, vol. cxiv., pp. 150, 263, 1897, bibliography. 
35 



Hoover, Am. Jour. 



546 



THE LIYEH. 



isms. ' These, entering the circulation, may pass the heart and pulmo- 
nary capillaries, with or without inducing lesions in the lungs, and, lodg- 
ing in the vessels of the liver, induce circumscribed necrosis of the liver 
tissue (see Fig. 40, page 113) and suppurative inflammation. Under 
these conditions we may find on a section of the liver larger and smaller 
yellowish or grayish spots, the larger of which may be soft and present 
the usual characters of abscesses. The smaller, which may not be larger 
than a pin's head, may present the usual consistence of liver tissue with 
the lobular structure still evident ; others may be softer, more yellow, 
and surrounded by a zone of hypersemic liver tissue. Microscopical ex- 
amination of the earlier stages often shows the blood-vessels filled with 
bacteria, scattered and in masses. Around these the liver cells are found 
in various stages of necrosis ; in many the nuclei do not stain and the 
bodies are very granular, or the entire cell is broken down into a mass 
of detritus. About these necrotic islets of liver cells pus cells collect 
and often form a zone of dense infiltration (Fig. 41, page 114). Thus, 
by the increase of pus cells and the necrosis of liver tissue, small ab- 
scesses are formed whose contents are intermingled with greater or less 
numbers of bacteria (Fig. 314), which seem to increase in number as the 
process goes on. By the confluence of small abscesses larger ones may 






i-'^i^ 



-'S 






^'^ 



-^-— , 







«":labSAi^f;|, 



':^ ^^flW^s^m^B^M''' ' 




Fig. 315.— Chronic Interstitial Hepatitis— Cirrhosis. 
a, New-formed connective tissue ; ft, dilated blood-vessels of the new tissue ; c, gall duct. 



be formed. Death usually ensues, however, before the abscesses attain 
a very large size. 

Chronic Interstitial Hepatitis (Cirrhosis). — The most marked result of 
chronic interstitial hepatitis is the formation of new connective tissue in 
the liver. The character, amount, and distribution of the new tissue 
vary greatly in different cases. Secondarily there are usually marked 

^ Kruse and Pasquale, Zeitschr. f. Hygiene u. Infkr., Bd. xvi., p. 1, 1894. 



THE LIVER. 



547 



changes in the liver cells and in the blood-vessels and gall ducts. The 
new tissue is most commonly formed and most abundant in the periph- 
erj' of the lobules along the so-called capsule of Glisson, but it may ex- 
tend into the lobules between the liver cells. It may surround single 
lobules, or more frequently larger and smaller groups of lobules (Fig. 




Fig. 316.— Chronic Interstitial Hepatitis— Cirrhosis. 

On account of the rough surface such livers are sometimes called " hob-nail livers, 
graphic reproduction of a cirrhotic liver of a child. 



This cut is a photo- 



315). It may occur in broad or narrow, irregular streaks or bands. 
It is frequently more abundant in one part of the liver than in another. 
The new-formed tissue tends to contract, and thus comj)romise by press- 
ure the enclosed islets of liver tissue, causing them to project, in larger 
and smaller nodules, from the surface of the organ. The liver cells may 
be flattened or atrophied from pressure ; or, from interference with the 
portal circulation, they may atrophy or become f^tty ; or they may be- 
come colored with bile pigment. This form of lesion is called atrophic 
cirrhosis. 

The varied appearances which cirrhotic livers present to the naked 
eye depend largely upon the amount and distribution of the new con- 
nective tissue and upon the secondary changes in the liver cells. The 
surface may be very rough and uneven from the projection of larger 



548 



THE LIVER. 



and smaller nodules of liver tissue (Fig. 316) or it may be quite smooth; 
or the organ may be greatly distorted by the contraction of large bands 
or masses of new connective tissue. In section through cirrhotic livers 
the new tissue may not be visible to the naked eye, or it may appear 
as grayish, irregular streaks, or bands, or patches, often sharply out- 
lined against the dark-red, or brown, or yellow, or greenish-yellow par- 
enchyma. When, as is often the case, fatty infiltration is associated 
with atrophic cirrhosis, the liver may not only not be diminished in size 
but may be larger than normal. 

On microscopical examination the new connective tissue is found in 




Fig. 317.— Chronic Interstitial Hepatitis. 

Showing a portion of the section shown in Fig. 315, but more highly magnifled. a. Portions of liver 
lobules ; h, new-formed connective tissue ; c, gall ducts, apparently new formed ; d, blood-vessels in the 
new tissue. 



some cases loose in texture and containing many variously shaped cells ; 
or it may be dense and contain comparatively few cells ; it is usually 
quite vascular. 

The new connective tissue' is most abundant between the liver lobules 
but it may encroach more or less upon their peripheries. Small gall 
ducts, some of them at least apparently new formed, are usually present 
in the connective tissue around the islets of parenchyma (Fig. 317). 
Some of these may usually be found continuous with the old ducts or 
gall capillaries. Sometimes rows of more or less cuboidal cells in the 

^ For a study of the character of the new connective tissue in cirrhosis see Flexner, 
University Medical Magazine, vol. xiii. , p./^13, 1900. 



THE LIVER. 



549 



connective tissue appear to be liver cells which have reverted to a sim- 
pler type (Fig. 318).' 

The branches of the hepatic and portal veins, particularly the latter, 
often become obliterated by pressure from the new connective tissue or 
from chronic thickening of their walls, so as seriously to interfere with 
the functions and nutrition of the liver cells. The bile ducts also may 
become obliterated, or there may be catarrhal inflammation, especially 
of the larger trunks. The branches of the hepatic artery are much less 
liable to alterations than the other vessels. The capsule of the liver 
is usually thickened, either uniformly or in irregular patches ; or its sur- 
face may be roughened by larger and 

smaller papillary projections. The ,^ : ^' 

liver is frequently bound to the dia- • "'^" , 

phragm or other adjacent organs by f . I. f» •' , , • 

connective -tissue adhesions. Amy- '^ ■; r" , * V ^' . , , . 

loid and fatty degeneration may be "" * > \ 

associated with cirrhosis. Cirrhotic 6 q Z- 

livers frequently show an unusual ^ .; . 

number of leucocytes in the blood- * '' '• ; -. ; 

vessels. -- ^' " • ''/ 

The obstruction to the portal cir- :^ c *« . . / 

culation induced by cirrhosis usually ^ '' i 

gives rise to a number of secondary - ^e^ ' ,, ^ '. 

lesions, since collateral circulation ^ , ^ 

is rarely established in sufficient de- 
gree to afford much relief. The 
hsemorrhoidal and vesical veins may 
be greatly enlarged, and also veins 
of communication between Glisson's 
capsule and the diaphragmatic veins. 

In rare cases a very peculiar dila- 
tation of the cutaneous veins about 
the umbilicus is observed. The en- 
larged veins form a circular network 

around the umbilicus, or a pyramidal tumor beside it, or all the veins 
of the abdominal wall, from the epigastrium to the inguinal region, 
are dilated. This condition is said to be dependent upon the congeni- 
tal non- closure and subsequent dilatation of the umbilical vein and its 
anastomoses with the internal mammary, epigastric, and cutaneous veins. 
According to'Sappey, it is not the umbilical vein which is dilated, but a 
vein which accompanies the ligamentum teres. 

There is very frequently also a dilatation of the veins of the abdomi- 
nal wall, which has a different origin. It is produced by the pressure of 
the fluid of ascites on the vena cava, and is found with ascites from any 
cause and with abdominal tumors. 

^ For a study of cell regeneration, reversion, etc., seeAdami, A. Jacobi's Festschrift, 
1900, p. 422. 



••»• 



Fig. 318. 



New-Formed Gall Ducts ix Cir- 
rhosis. 



The section shows the projection into the new 
connective tissue from the rows of old liver cells, 
of cell masses resembling gall-duct epithelium. 
This may be interpreted as an example of rever- 
sion of the differentiated liver cells to a simpler 
type. 



550 



THE LIYEE. 



Ascites is the most common secondary lesion of atrophic cirrhosis. 
It usually begins at an early stage of the disease, and is apt to increase 
constantly. It generally precedes oedema of the feet, but both may ap- 
pear at the same time. This fluid is of a clear yellow or brown, green 
or red ; it is sometimes mixed with shreds of fibrin, and more rarely 
with blood. The peritoneum remains normal, or becomes opaque and 
thick, or there may be adhesions between the viscera. 

The spleen is very frequently enlarged, and the enlargement may be 
considerable. When it is not increased in size this seems usually due 
to previous atrophy of the organ, or to fibrous thickening of its capsule, 
or to haemorrhages from the stomach and bowels occurring just before 
death. 

The stomach and intestines are often secondarily affected by the ob- 
struction to the portal circulation. Profuse haemorrhage from the stom- 
ach and intestines may occur and sometimes cause sudden death. The 
mucous membrane is then found pale, or congested, or with hsemor- 
rhagic erosions. The haemorrhage not infrequently results from rupture 
of oesophageal varices which are present, especially in the lower portion, 
in a noteworthy proportion of cases of atrophic cirrhosis. ^ Sometimes 
the blood is infiltrated in the coats of the stomach and intestines. 

The mucous membrane of the stomach, and of the entire length of the 
intestines, is frequently the seat of chronic catarrhal inflammation, and 
is sometimes uniformly and intensely congested and coated with mucus. 
In other cases both the mucous and muscular coats are pale, but very 
markedly thickened. 

Cirrhosis of the liver is not infrequently accompanied by chronic dif- 
fuse nephritis. 

Hypertrophic Cirrhosis. — There is a form of interstitial hepatitis in 
which the growth of new tissue occurs not only between the lobules but 
extends into the lobule between the liver cells (Fig. 319). Under these 
conditions even in advanced forms of the lesion the liver may be en- 
larged, the surface may be smooth or slightly roughened, the parenchyma 
is often bile-stained. This form of interstitial hepatitis is called hyper- 
trophic cirrhosis. There is a form of interstitial hepatitis, usually of the 
hypertrophic type, in which the growth of connective tissue is most 
marked in the vicinity of the smaller bile ducts. This often occurs in 
connection with obstruction of the bile ducts and the lesion is called Mili- 
ary cirrhosis. In ^^ biliary cirrhosis'^ marked jaundice is said to be com- 
mon while ascites is moderate or absent. In certain cases there is a 
marked difl'erence in the gross and microscopic appearance in atrophic 
and hy j)ertrophic cirrhosis, but intermediate forms occur. The difference 
in the conditions which lead to these two forms of cirrhosis of the liver, 
the atrophic and the hypertrophic, is not yet clear, and the distinctions 
which have been made between them, in part clinical, in part morpho- 
logical, are often unsatisfactory. 

^ For a critical summary of gastro -intestinal haemorrhage in cirrhosis with bibliog- 
raphy see Prehle, Am. Jour. Med. Sciences, vol. cxix., p. 263, 1900. 



THE LIVER. 551 

The causes of cirrhosis are imperfectly understood. It is a disease 
of adult life, but exceptionally occurs in children. Congenital cirrhosis 
with obliteration of the bile duct is of occasional occurrence.' In 
adults it seems in many cases to be directly dependent upon the contin- 
ued ingestion of large quantities of strong alcoholic liquors. It very 
rarely occurs as a result of beer drinking. There are many cases of cir- 
rhosis for which no cause can be discovered.^ It is probable that in cer- 
tain cases at least a degeneration of circumscribed areas of liver paren- 
chyma precedes and probably determines the new formation of connective 
tissue; the lesion would then be more properly considered a replace- 
ment hyperplasia than as strictly inflammatory. ^ 

Welch ^ has described the occurrence of small circumscribed areas of 





9 --;/ 











Fifi. 319.— Hypertrophic Cirrhosis of the Liver. 
Showing formation of connective tissue between the liver cells. 

fibrous tissue in the liver, replacing liver cells and containing coal pig- 
ment. This rare lesion he has called cirrhosis hepatis anthracotica. 

Syphilitic Hepatitis. — Chronic interstitial inflammation of the liver 
very frequently results from syphilitic infection, either congenitally or 
in the later stages of the acquired form. It may occur in a diffuse man- 
ner, new connective tissue being formed either between the lobules, or 
within them between the rows of liver cells. The new tissue may be 
rich in cells, or dense and firm. This form is frequently seen in chil- 
dren, and cannot be distinguished, either macroscopically or micro- 
scopically, from similar forms of interstitial hepatitis from other causes. 

^ See Bolleston and Hayne, British Med. Jour., 1901, vol. i., p. 758, bibliography. 

-For a study of experimental cirrhosis of the liver see v. Heukelom, Ziegler's Beitr., 
Bd. XX., p. 221/1896, bibliography. 

■^ For a study of the germicidal capacities of the liver and the possible relationship 
of latent or subinfection to cirrhosis see Adami, Jour., Am. Med. Asso., Dec. 16th and 
23d, 1899, bibliography. 

■* Welch, " Cirrhosis hepatis anthracotica, " Johns Hopkins Hospital Bulletin, vol 
ii., p. 32, 1891. 



552 



THE LIVER. 



In other cases, particularly in children, there may be numerous 
small gummata (so-called miliary gummata) (Fig. 125, page 234) scat- 
tered through the liver, together with more or less new connective tis- 
sue. In adults gummata are usually larger, varying in size from that of 
a pea to a hen's Qgg, and may be surrounded by larger and smaller irreg- 
ular zones of ordinary connective tissue (Fig. 320). In still other cases 
in adults there are larger and smaller dense, irregular bands or masses 
of connective tissue running through the liver, drawing in the capsule 
and often causing great deformity of the organ. These bands and masses 
of new tissue may or may not enclose gummata, either large or small. 




Fig. 320.— Gumma of Liver. 

a. Cheesy centre ; b, fibrous periphery ; c, small-celled peripheral Infiltration ; d, portions of live lobules. 
The drawing is somewhat schematic. 



These deforming cicatrices, either with or without gummata, are very 
characteristic of syphilitic inflammation of the liver. 

This, like the simple interstitial inflammation of the liver, may be 
associated with fatty and waxy degeneration, and with atrophy of the 
parenchyma from pressure. 

Tuberculous Hepatitis. — This lesion, which is usually secondary to 
tuberculous inflammation in some other part of the body, or a part of 
acute general miliary tuberculosis, is most frequently characterized by 
the formation of larger and smaller miliary tubercles, which may be 
either within or between the liver lobules or in the walls of the bile 
ducts. Many of the tubercles are too small to be seen with the naked 
eye; others may be just visible as grayish points; still others may 
be from 1 to 3 mm. in diameter, with distinct yellowish -white cen- 
tres. Microscopical examination shows considerable variation in the 
structure of the tubercles in different cases, as well as in the same liver. 
Some of them, usually the smaller ones, consist simply of more or less 



THE LIVER. 553 

circumscribed collections of small spheroidal cells, which are not mor- 
phologically distinguishable, so far as the form and arrangement of the 
cells are concerned, from simple inflammatory foci, or from the diffuse 
masses of lymphatic tissue which occur normally in the liver. 

In other forms we find a well-marked reticulum with larger and 
smaller spheroidal and polyhedral cells, with or without giant cells. In 
still other forms there is more or less extensive cheesy degeneration. 
The larger forms are conglomerate, being composed of several tubercle 
granula joined together to form a single nodular mass. The liver cells 
at the seat of the tubercle are destroyed, and the interstitial tissue and 
blood-vessels are either destroyed or merged into the tubercle tissue. In 
the periphery of the tubercles the liver cells may be in a condition of 
coagulation necrosis, and the tissue round about may be infiltrated with 
small spheroidal cells. There is in some cases a new formation of gall 
ducts or of structures which resemble these, and which in transverse sec- 
tions resemble giant cells. Tubercle bacilli, frequently in small numbers, 
but often in great abundance, may be found within the tubercles. 

Tuberculosis of the liver may be associated with cirrhosis, or waxy 
and fatty degeneration. 

Much more rarely than the above form there are found in the liver 
more or less numerous scattered tuberculous masses from the size of a pea 
to that of a walnut or larger, with cheesy centres and usually a new 
growth of connective tissue in the peri^Dhery. These so-called solitary 
tubercles of the liver may be softened at the centres. Tuberculous inflam- 
mation of the gall ducts may give rise to numerous scattered, cheesy 
nodules, as large as a pea or larger, which may be softened at the centre 
and stained yellow with bile. Small cavities may thus be formed.' 
This lesion is rare and seems to be more frequent in children than in 
adults. 

Perihepatitis. — Acute exudative inflammation of the serous covering of 
the liver, with the formation of fibrin, may occur as a part of acute gen- 
eral or localized peritonitis, or over the surface of abscesses, tumors, 
hydatids, etc. , of the organ, when these lie near or approach the surface ; 
or it may be secondary to acute pleurisy. 

Chronic xjeriliepatitis, resulting in the thickening of and formation of 
new connective tissue in and beneath the capsule of the liver, may be 
secondary to an acute inflammation of the capsule, or it may be chronic 
from the beginning and associated with chronic pleurisy, chronic peri- 
tonitis, and .cirrhosis. In this way more or less extensive adhesions of 
the liver to adjacent structures may be formed; or, by contraction of the 
new-formed connective tissue, considerable deformity of the liver may 
be produced. The capsule is sometimes uniformly thickened, sometimes 
the new tissue occurs in more or less sharply circumscribed patches. The 
surface is sometimes roughened from little, irregular projecting masses 
of connective tissue. Microscopically the new-formed tissue is usually 

^ See for a stud^y of tuberculous cavities in the liver, Fletcher, Journal of Pathology 
and Bacteriology, vol. vi., p. 147, 1900, bibl. 



554 THE LIVER. 

dense and firm, but it may be loose in texture and contain many cells. 
^N'ot infrequently bands or masses of connective tissue run inward from 
the thickened capsule between the superficial lobules, causing localized 
atrophy of the parenchyma. 



HYPERPLASIA OF LYMPHATIC TISSUE IN THE LIVER. 

In some forms of leukaemia and pseudo- leukaemia the liver is not in- 
frequently enlarged and soft and besprinkled with small white spots, or 
streaked with narrow whitish, irregular bands, or it may be of a diffuse 
grayish color. Microscopical examination shows this change to be due 
to an accumulation of cells resembling leucocytes, either along the portal 
vein, or diffusely through the liver tissue, or in small circumscribed 
masses. The amount of accumulation of these small cells varies much, 
but is sometimes so great as seriously to compromise the liver cells. The 
origin of these new cells is not yet definitely known. They may be, and 
doubtless in part are, brought to the organ through the portal vein ; but 
they may, in part at least, be formed in the liver itself, possibly from 
the capillary endothelium. 

In typhoid fever, smallpox, scarlatina, diphtheria, and measles small 
circumscribed masses of spheroidal cells are sometimes found in the 
liver. These nodules differ in character, some are due to focal necroses, 
such as occur in various toxaemias with a later multiplication of cells or 
invasion of leucocytes. In some, as in typhoid fever, there is necrosis 
with proliferation of endothelium (see page 209). Finally some of the 
small masses of spheroidal cells encountered in the liver in infectious 
diseases are doubtless hyperplastic lymph-nodules. ' 



TUMORS OF THE LIVER. 

Tumors of the liver may be primary or secondary ; the latter are most 
common. 

Cavernous Angiomata. — These tumors, usually small, are most common 
in elderly persons and are of no practical significance. They may be 
situated at the surface or embedded in the organ, and are of a dark -red 
color ; sometimes sharply circumscribed by a connective -tissue capsule, 
sometimes merging imperceptibly into the adjacent liver tissue. Micro- 
scopically they consist of a congeries of irregular cavities (Fig. 169, page 
303) filled with blood and frequently communicating freely with one 
another. The walls of the cavities consist of connective tissue, often 
containing small blood-vessels, and are sometimes thick, sometimes thin. 
They are believed to be formed by dilatation of the liver capillaries, with 
subsequent thickening of their walls and atrophy of the adjacent liver 
cells. 

^ For changes in the blood in diseases of tlie liver consult Mwing's "Clinical Pathol- 
ogy of the Blood." 



THE LIVER. 555 

Small fibromata and lipomata have been described, also fibroneuromata 
of the sympathetic. 

Adenomata of the liver are of not infrequent occurrence. They are 
sometimes small and circumscribed, sometimes very large and multiple. 
They present two tolerably distinct types of structure. In one form the 
tissue presents essentially the same structure as normal liver tissue, ex- 
cept that the arrangement of the cells is less uniform and the cells are 
apt to be larger. They look like little islets of liver tissue, sometimes 
encapsulated and sometimes not, lying in the liver parenchyma. In the 
other form the cells are less like liver cells, are frequently cylindrical, 
and are arranged in the form of irregular masses of tubular structures 
with more or less well-defined lumina. These tumors are sometimes 
large and multiple, and in one case described by Greenfield there were 
metastatic tumors in the lungs. These tubular adenomata are in some 
cases so closely similar to some of the carcinomata as to be scarcely dis- 
tinguishable from them, and seem, indeed, to merge into them. ^ 

Aberrant nodules of adrenal tissue have been found in the liver and 
may be mistaken for adenomata. Cysts may develop in adenomata. ^ 

Carcinomata are the most common and important of the liver tumors, 
and may be primary and secondary. Primary carcinomata of the liver are 
probably developed from the epithelium of the gall ducts, and in some 
cases are arranged along the larger trunks. The cells are usually poly- 
hedral, sometimes cylindrical, and may be arranged irregularly in alveoli 
or form more or less well-defined tubular structures. 

Secondary carcinoma of the liver, which is by far the most common, is 
usually due to the dissemination in the organ of tumor cells from carci- 
nomata of the stomach, intestines, pancreas, or gall bladder. But it 
may be the result of metastases from the mamma, oesophagus, uterus, 
and various other parts of the hodj. In secondary carcinoma the cells 
resemble more or less closely the type of those forming the primary tumor. 

The form in which the carcinoma in the liver occurs varies consider- 
ably. Sometimes the tumors are single, but more often multiple (Fig. 
321) ; they may be very large, or so small as to be scarcely visible to the 
naked eye ; very frequently numerous small nodules are grouped in the 
periphery of a larger one. They are sometimes deeply embedded in the 
liver, sometimes they project from the surface. The liver is frequently 
and sometimes enormously enlarged. The nodules are usually whitish or 
yellowish or pink in color or bile-stained, and they are often the seat of 
haemorrhages^- and may become softened at the centre, forming cysts filled 
with degenerated tumor tissue often mixed with blood. The nodules are 
sometimes hard, sometimes soft and almost diffluent. Fatty degenera- 
tion in the tumor is frequent, and may be recognized by yellowish streaks 
or j)atches on the sections. Owing to the degeneration and partial absorj)- 

' SokoloffhsiS described an adeno-careinoma of the liver with ciliated cells, Virchow's 
Arch., Bd. clxii., p. 1, bibliography of allied tumors. 

- See for cyst formation in the liver DmocJiowski and JanowsM, Ziegler's Beitr. z. 
path. Anat., Bd. xvi., p. 102. 



556 THE LIVER. 

tion of the central portions of the tumors, the nodules on the surface of 
the liver frequently present a shallow depression at the centre. The 
tumors may be sharply outlined against the adjacent liver tissue, or may 
merge imperceptibly into it. They may be so large or numerous as to 
occupy the greater part of the enlarged organ. The neighboring liver 
cells may be flattened and atrophic. The tumors may press upon the 
portal vein or its branches, or upon the gall ducts, and thus seriously 
interfere with the functions of the organ. Sometimes, however, the 
tumors are very large and numerous without apparent interference with 
the function of the liver. Melanotic carcinomata sometimes occur in the 
liver, most frequently as secondary tumors. 

In some cases, instead of forming separate, distinct nodules, the can- 
cerous growth develops in the form of a diffuse infiltration of the organ, 
so that the often greatly enlarged liver is irregularly mottled with white 
and reddish-brown masses, and may then somewhat resemble some forms 
of chronic interstitial hepatitis. 

Sarcomata. — Spindle-celled, melanotic, and telangiectatic sarcomata 
may occur in the liver as secoudary tumors.' Secondary myxomata and 
chondromata have also been described, but they are very rare. Angiosar- 
coma may occur as a primary tumor. ^ 

Cavernous lymphang-iomata have been described in a few cases. Cysts, 
usually of small size, may be formed by dilatation of the bile ducts. They 







Fig. 321.— Secondary Carcinoma of the Liter. 

The section is through the entire organ, showing carcinomatous tumors of various sizes and forms : 
some are white, some are dark red from haemorrhage. The larger tumor at the left is softening at the 
centre. 

may be multiple and contain serum, mucus, and degenerated epithelium. 

Single cysts, apparently unconnected with the gall ducts, are occasionally 

found in the connective tissue of the liver. They may be lined with 

ciliated epithelium. 

The liver is sometimes the seat of larger and smaller multiple cysts, 

^ See Hektoen and Herrick, Trans. Assn. Am. Phj^s., vol. xiii., p. 385, 1898, 
^Arnold, Ziegler's Beitr. z. path. Anat., Bd. viii., p. 123. 



THE LITER. 557 

varying from microscopical size up to that of a pea, and sometimes larger. 
They do not appear to communicate with the gall ducts. They are some- 
times associated with multiple cysts of the kidney. Their origin and 




Fig. 322.— "Foamy Liver."' 

The liver is riddled with small holes formed by the accumulation of gas developed by B. aerogenes capsula- 

tus— ''gas bacillus." 

nature are not understood, but they are probably congenital. A teratoma 
of the liver has been described by Misick. ' 

Occasionally the liver is found at the autopsy, even if this be made 
but a few hours after death, more or less completely riddled with small, 
irregular-shaped cavities, from the size of a pin's head to that of a pea 
(Fig. 322) . These holes are due to the accumulation of gases in the liver, 
formed by the Bacillus aerogenes capsulatus. This is the so-called 
^^ foamy liver ^' (see page 243). 

PARASITES. 

Echinococcus. — This parasite is the most common and important of 
those which occur in the human liver. It forms the so-called hydatids of 
the liver. These represent one of the developmental stages of the small 
tapeworm of the dog, Tcenia ecMnococcus (see page 132). The cysts in 
the liver may be very small and multii)le, but they may be as large as 
a man's head or larger. The liver may be greatly increased in size, and 
the tissue about the cysts atrophied. The liver itself furnishes a connec- 
tive-tissue capsule, within which is the translucent, lamellated membrane 
furnished by the parasite. On the inside of this we may find a layer of 
cells, granular matter, and a vascular and muscular system belonging to 
the parasite. Projecting from this inner capsule are the brood capsules 
and heads or scolices of the immature tapeworm. The scolices may be- 
come detached from the wall and lie free in the cavity, which is filled 
with a transparent or turbid fluid. Not infrequently the cysts are 
sterile, and are then simply filled with clear or turbid fluid ; or the em- 
^ Misick, Jour. Path, and Bact., vol. v., p. 128, 1898. 



558 THE LIYEE. 

bryos may have died and disintegrated, and their detritus, including the 
hooklets, may be intermingled with the fluid contents of the cysts. The 
contents of the cysts may be mixed with fat, cholesterin crystals, pus, 
bile, or blood ; or form a grumous mass, in which we may or may not 
be able to find the hooklets of the scolices or fragments of the lamellated 
wall. The connective tissue of the walls of the cysts may be greatly 
thickened, or they may be calcified. 

In other countries the lesion is much more common and frequently 
more formidable than in the United States. The cysts reach an enor- 
mous size, the veins of the liver may be compressed and filled with thrombi, 
the bile ducts compressed and ulcerated. So much of the liver tissue 
may be replaced by the hydatids that the patient may die from this cause 
alone. Very frequently there is local peritonitis, and adhesions are 



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Fig. 323.— Echixococcus Multilocularis of the Liver, 

A section of a small portion of the cystic and fibrous growth in the liver. There were no hooklets 
within the cysts in this case, but the delicately lamellated character of the lining membrane sufficed for a 
diagnosis. 

formed between the liver and the surrounding parts. In some cases the 
cysts rupture, and their contents are emptied into the peritoneal cavity, 
the stomach, the intestines, the pleural cavity, or the lung tissue. Some- 
times the cysts perforate the bile ducts, the vena cava, or some of the 
branches of the portal or hepatic veins ; or the abdominal wall is perfo- 
rated and a fistula formed between the cavity in the liver and the surface. 

Echinococcus multilocularis (see page 134), which is apparently an 
abortive form of the above species, is very rare in the United States 
(Fig. 323).^ 

Distoma hepaticum, D, sinense, D. lanceolatum, may occur in the gall 
ducts and gall bladder. D, sinense occurs especially in the East, and has 
been found in great numbers in the bodies of Chinamen. D. haematobium 
is very common in Egypt and Abyssinia, occurring in the blood-vessels 
of the liver. 

^See Oertel, Yale Medical Journal, vol. v., p. 233, 1899; consult also monograph 
by Posselt, 1900. 



THE LIYEE. 559 

Pentastoma denticulatum is the undeveloped form of Pentastoma 
tsenioides, a parasite which inhabits the nasal cavity of dogs and some 
other animals. In the liver of man it usually occurs in the form of 
small, rounded, calcified cysts. The cysts may contain fat, calcareous 
matter, and the remains of the dead parasite, among which the hooklets 
may be found. 

Ascaris lumbricoides sometimes finds its way from the intestines into 
the bile ducts. It may cause no disturbance here, but in some cases the 
worms have been present in large numbers and caused occlusion, dilata- 
tion, and ulceration of the biliary passages, and have led to the forma- 
tion of abscess of the liver. 

Coccidium oviforme, the very common parasite in the rabbit's liver, 
has been found a few times in the liver of man. 



LESIONS OF THE BILIARY PASSAGES AND THE GALL 

BLADDER. 

Perforation and rupture of the gall bladder may occur under various 
conditions and is usually followed by peritonitis. ^ 

Catarrhal Inflammation most frequently involves the lower portion of 
the common duct and the gall bladder. In the acute form it usually 
leaves but few changes appreciable after death. An abnormal coating 
of mucus, and sometimes congestion of the blood-vessels, are almost the 
only post-mortem lesions. Owing to the swelling of the mucous mem- 
brane and the accumulation of mucus in the lumen, the ducts may be 
temporarily occluded, but this occlusion may not be evident after death. 
If, however, the inflammation becomes chronic, the walls of the bile 
ducts may become thickened and their lumina more or less permanently 
obstructed. In consequence of this, dilatation or ulceration of the bile 
ducts may ensue. Temporary obstruction of the bile ducts may pro- 
duce marked jDigmentation of the liver, owing to the accumulation of 
pigment granules in the liver cells, particularly in the vicinity of the 
capsule of Glisson, and jaundice of the entire body. 

The gcdl Madder may be inflamed by itself — cholecystitis — or in connec- 
tion with inflammation of the biliary passages. If the disease is chronic 
the wall of the bladder may be thickened ; polypoid growths may occur 
in the mucosa; the duct may be occluded; dilatation, ulceration, the 
formation of gall stones, calcification, and atrophy may ensue. 

Inflammation of the stomach and duodenum, hypersemia and inflam- 
mation of the liver, concretions, and parasites frequently accompany 
catarrhal inflammation of the biliary passages, but it may occur without 
these. 

Suppurative and Croupous Inflammation of the Bile Ducts (Cholangitis) 
and Gall Bladder (Cholecystitis). — The walls of the ducts maybe covered or 
infiltrated with a fibrinous or a purulent exudate ; they may ulcerate. 

^ See MacJiard, Arch. gen. de Med., t. iv., p. 159, 1900, bibliography. 



560 THE LIVER. 

These lesions occur most frequently in connection with obstruction of 
the bile ducts by gall stones or otherwise, and in typhoid and typhus 
fever, pysemia, and cholera ; or they may be due to the extension of 
inflammatory processes from without. They also occur under unknown 
conditions. 

In many cases of inflammation of the gall ducts, the Bacillus coli 
communis, in fewer, the pyogenic streptococcus and staphylococcus are 
apparently concerned. 

Suppurative inflammation may lead to perforations of the ducts or 
bladder, with escape of bile and peritonitis ; or fistulous openings be- 
tween the gall bladder and the duodenum, colon, and stomach, or through 




Fig. 334.— Suppurative Inflammation of the Gall Ducts in the Liver— Cholangitis. 

The suppurative foci are almost coalescent in the infected region. This lesion was secondary to suppura- 
tive inflammation in the larger gall passages with the presence of gall stones. 

the abdominal wall. Or the inflammation may extend to the liver tissue 
and prod^x^e abscesses. Under the latter conditions we may find a series 
of small abscesses ranged along the walls of the suppurating gall ducts 
(Fig. 324). In more advanced stages the abscesses may become large 
and communicate with with one another, so that a considerable portion 
of the liver may be occupied by a series of communicating cavities with 
ragged walls, containing pus and detritus of liver tissue more or less 
tinged with bile. 

Such abscesses may become more or less completely enclosed by con- 
nective-tissue walls. The portal vein may also become inflamed, and 
perforations may be formed between it and the bile ducts. The excitants 
of these inflammatory processes in the gall ducts and gall bladder are 
probably usually bacteria. Those which have been most frequently 



THE LIVER. 561 

found are the ^^ pyogenic cocci/^ ' the colon and typhoid bacilli, and the 
pnenmococcus. It should be borne in mind that post-mortem invasion 
of the gall bladder and passages by bacteria may take place early. 

Constriction and Occlusion of the Bile Ducts. — This may be produced by 
inflammation of the ducts themselves, by new growths in their walls, by 
calculi or parasites in their lumina, by changes in the hepatic tissue in 
chronic and acute hepatitis, by aneurisms, or by pressure on the duct 
from without, as by tumors in the head of the pancreas, etc. 

The obliteration of the smaller bile ducts produces no marked lesions. 
When the ductus communis or the hepatic duct is obstructed, the ducts 
throughout the liver are frequently dilated and the liver tissue is bile- 
stained. The liver may undergo atrophy and the whole body be in- 
tensely jaundiced. When the cystic duct is obstructed the gall bladder 
is dilated. 

Dilatation of the Bile Ducts is usually produced by strictures in the 
ways just mentioned, or by calculi. When calculi have produced the 
dilatation this condition may sometimes continue after they have found 
their way into the intestines. Sometimes, however, we meet with very 
marked dilatation of the bile ducts without being able to make out any 
present or past obstruction. The dilatation may affect only the common 
and hepatic ducts, or it may extend to the smaller ducts in the liver, 
which are then dilated uniformly or in sacculated forms. They may con- 
tain bile, mucus, or calculi. The liver is at first enlarged, but may after- 
ward atrophy. The gall-bladder may be dilated in consequence of obstruc- 
tion of the common or the cystic duct. In the latter case it may reach an 
immense size and form a large tumor in the abdominal cavity. The 
dilatation is generally uniform, the bladder retaining its normal shape ; 
sometimes, however, there are diverticula, which are usually produced 
by calculi. If the obstruction to the hepatic duct is incomplete or mov- 
able the gall bladder may contain bile, and often calculi. If the obstruc- 
tion is complete the contained fluid may gradually lose its biliary char- 
acter and become a serous or mucus fluid of a light-yellow color — hydrops 
cijstidis fellecB. The walls of the bladder may be of normal thickness, or 
thinned, or thickened, or calcified. If the obstruction is due to a cal- 
culus, this may pass into the intestine and the gall bladder be suddenly 
emptied. Usually the bladder fills again, owing to its loss of contractile 
power. 



TUMORS OF THE GALL BLADDER AND LARGER GALL DUCTS. 

Small fibromata have been described in the gall bladder and in the 
common duct, but they are a ery rare. The most common tumors are 
carcinomata. These may be primary or secondary, and present the usual 
structural A^ariations. The cells may be cylindrical, or polyhedral ; or 
they may present the characteristics of gelatinous cancer. Primary carci- 

^ For a study of gall-bladder infections consult CusMng, Johns Hopkins Hosp. 
Bull., vol. X., p. 166, 1899, bibliography. 
36 



562 THE LIVER. 

nomata and adenocarcinoma of tlie gall bladder and larger gall ducts are 
not uncommon, and are frequently associated with calculi. ' Kot infre- 
quently the pancreatic and common ducts are both involved, and it is 
difficult to say whether the tumor is primary in the head of the pancreas 
or in the gall duct. The bladder and ducts may also be secondarily in- 



/f 









, .% 




Fig. 325.— Adenoma of the Gall Duct. 
This section is from a small tumor growing within one of the larger gall ducts in the liver. 

volved in carcinomata of the stomach, liver, and duodenum. Adenoma 
of the gall ducts is of occasional occurrence (Fig. 325). 

BILIARY CALCULI. (Cholelithiasis.) 

These bodies are of common occurrence. They are found usually in 
the gall bladder, sometimes in the hepatic, cystic, and common ducts ; 
less frequently in the small ducts of the liver. In the gall bladder from 
1 to 7,800 calculi have been counted. They vary in size from that of a 
pin's head to that of a hen's egg, or they may be larger. Single gall 
stones are usually spheroidal or ovoidal ; when multiple they are usually 
flattened at the sides or faceted. 

They may be composed : 

1. Principally of cholesterin, and may be of pure white color, or 
tinged with various shades of yellow or brown by bile pigment. The 
fractured surface shows a radiating crystalline structure. 

2. Of cholesterin, bile pigment, and salts of calcium and magnesium. 

^See Warthin, Philadelphia Med. Journal, vol. vi., pp. 38, 82, and 120, 1900, bib 
liograpby. 



THE LITER. 563 

These are usually dark -colored, brown, reddish-black, or green, and may 
be spheroidal or faceted, smooth or rough on the surface ; the fractured 
surface is usually radiating crystalline. This is the most common form. 

3. Principally of hile pigment. Such calculi are rare, usually small, 
very dark- colored, and not numerous. 

4. Of calcium carl)onate. These are rare, have a nodular surf ace, and 
a clear crystalline, not radiating fracture. 

Most calculi are formed around a central mass, sometimes called the 
nucleus, which may consist of cholesterin, bile pigment, mucus, or epi- 
thelium, or more rarely of some foreign body. Thus a dead parasite, a 
needle, and fruit seeds may serve as nuclei. The body of the calculus 
may be homogeneous, or lamellated, or crystalline. 

Biliary calculi in the gall bladder may produce no symptoms and be 
discovered only after death. In the hepatic and common ducts they may 
obstruct the flow of bile and lead to fatal jaundice ; or they may pass 
from time to time into the intestine, iDroducing biliary colic. If they 
are impacted in the cystic duct they may lead to dilatation of the gall 
bladder. They may get into the duodenum by ulceration through the 
walls of the ducts or gall bladder, or in the same way into the peritoneal 
cavity. Gall stones which get into the intestinal cavity usually pass off 
without doing any further injury, but very large calculi may cause oc- 
clusion of the gut with fatal results. The role of micro-organisms in the 
formation of gall stones has been the subject of significant studies.' 

' Con9,vi\t Mignot, Arch. gen. de Medecine, 1898, t. ii., pp. 129 and 263; also CusMng, 
Johns Hopkins Hosp. Bull., vol. x., p. 166, 1899; also Mieczkowski, Mitth. a. d. Grenz- 
geb. d. Med. u. Chlr., Bd. vi., p. 307, 1900. 




• - CHAPTER IX. 

THE URINARY ORGANSo 

The Kidneys. 

Malformations. 

Both kidneys may be absent in connection with extensive malformation in foetuses 
which are. not viable. 

Abs&nce of one kidney is not uncommon, the left kidney being more frequently 
absent than theii right. The absence of the kidney may be complete, the ureter being 
also absent; there may be an irregular mass of much-atrophied kidney tissue with con- 
nective tissue and fat, or there may be only a little mass of connective tissue and fat 
representing the kidney, and a ureter running down to the bladder. The single kidney 
which is present is usually much enlarged. It may be in its natural position or dis- 
placed downward. 

When both kidneys are present one of them may be much larger than the other. 
One kidney may have two pelves or two ureters. 

A frequent malformation is the so-called Jiorseslioe kidney. The lower ends of the 
kidneys are joined together by a commissure. The commissure is usually composed of 
kidney tissue, but sometimes of connective tissue. The two kidneys may be normal, 
except for the commissure ; or their shape, the arrangement of the vessels and ureters, 
and the position, may be unnatural. The two kidneys may be united throughout so 
as to look like a single misshapen kidney with two or more pelves and irregular blood- 
vessels. The united kidneys may be both situated on one side of the vertebral column 
or in the pelvis. 

Changes in Position. 

The kidneys may be placed in an abnormal situation, in which they are either fixed 
or movable. 

The change in position is either lateral or downward. When displaced downward 
the kidney may be over the sacrum or below this in the cavity of the pelvis. The ves- 
sels also have an irregular origin and distribution. The kidney is firmly attached in its 
abnormal position. 

Movable or wandering kidneys are found in adult life as a result of tight lacing, 
of pregnancy, of overexertion, and of unknown causes. They are more common in 
females than in males, and the right kidney is most frequently involved. The blood- 
vessels become lengthened and the attachments of the kidney longer and looser. 

COMPENSATORY HYPERTROPHY OF THE KIDNEY. 

When one kidney is involved in lesions which serionsly interfere with 
its function the other organ may increase in functional capacity through 
an hypertrophy and hyperplasia of its gland cells. A similar alteration 
may take place in the sound parts of an organ partially compromised by 
structural lesions. * 

^For a study of this condition see Sacerdotti, Virchow's Arch., Bd. cxlvi., p. 267, 
1896, bibliography. 

Consult also for general consideration of hypertrophy Thoma, " Text-Book of Gen- 
eral Pathology," vol. i., p. 448, English translation. 



THE UEINAEY OH&ANS. 565 



DISTURBANCES OF CIRCULATION. 

Anaemia of the kidney occurs in general anaemia : it may be associated 
with various forms of diffuse nephritis. Local anaemia may be due to 
thrombosis or embolism. 

Acute Hyperaemia — Acute Congestion. — This may occur in early phases 
of an acute inflammatory process or after the ingestion of irritant poisons. 
The kidneys may be swollen, the vessels distended, and bloody fluid ex- 
udes from the cut surfaces. There may be extravasation of red blood 
cells from diapedesis. 

Chronic Hyperaemia — Chronic Congestion. — This may occur in connec- 
tion with a similar condition in the other viscera when the circulation is 
impeded through uncompensated lesions of the heart and lungs, such as 
chronic endocarditis involving the aortic and mitral valves, cardiac dila- 
tation, aortic aneurism, emphysema, large accumulations of fluid in the 
pleural cavities ; or it may be associated with obstruction of the renal 
vein or inferior vena cava by thrombosis or pressure from tumors, etc. 
The kidneys in this condition are, when typical, slightly or considerably 
enlarged, increased in weight, hard, and dark red in color with capsule 
not adherent and surface smooth. The congestion is most marked in the 
capillaries of the glomeruli which are widely dilated, often with thickened 
walls ; in the interlobular veins, the vasa recta, and the stellate veins of 
the cortical surface. 

The epithelium of the convoluted tubules may be swollen ; or it may be 
much flattened so that the lumen of the tubule is enlarged. If the con- 
gestion persist, there is hyperplasia of the interstitial tissue of the kidney 
with degeneration of the epithelium, the formation of casts, atrophy of 
the tubules, etc. Chronic congestion may lead to chronic diffuse nephritis. 

Embolism, Thrombosis, and Infarction. — If the renal artery or one of its 
branches be plugged by an embolus or thrombus, an anaemic infarction 
of the region is the result. There may be one or several such infarctions 
which are usually more or less wedge-shaped, the apex directed inward 
corresponding to the vascular territory comi)romised. They are pale or 
yellowish, hard, and as inflammatory reaction sets in may be surrounded 
by a red hyperaemic zone. 

Within the limits of the infarction, necrosis of epithelium or of the 
entire mass of " involved tissue may take place with such subsequent 
alterations as have been already described on page 76. 

The seat of old and healed infarctions may be indicated by small 
fibrous cicatrices. * 

Haemorrhagic infarctions in the kidney are rare. Infarctions may 
become the seat of gangrene when putrefactive bacteria gain access to 
them ; or suppurative inflammation with the formation of abscesses may 
occur. Embolism of the renal artery may result in necrosis of the entire 

' For a study of the regenerative capacity of the renal epithelium in infarctions see 
Tliorel, Virchow's Arch., Bd. cxlvi., p. 297, 1896, bibliography. 



566 THE URINARY ORGANS. 

kidney. Thrombosis of the renal vein may be induced by the pressure 
of tumors, either on this vessel or on the vena cava ; or it may occur in 
cachectic conditions. 

ALBUMINURIA AND CASTS. 

Albuminuria. — Albuminous material or serum not infrequently passes 
out of the blood-vessels of the kidneys, either through the glomeruli or 
the tubules, and mingles with the excreted substances. While this may 
occasionally occur under conditions which cannot be regarded as ab- 
normal, it is common in many diseases of the kidney and is frequent 
without demonstrable kidney lesions in fevers, infectious diseases, ab- 
normal conditions of the blood, various forms of poisoning, disturbances 
of the circulation, etc. Albuminous material may also be set free by 
abnormal metabolism or disintegration of the renal epithelium. 

In albuminuria with pronounced kidney lesions there are usually 
well-defined alterations in the capillaries of the tufts and in their epi- 
thelial investment. There may be thrombi in the capillaries ; their walls 
may be thickened ; the flat epithelium covering them may be swollen or 
fatty, or may peel off, or it may proliferate. In the kidneys of cases of 
pronounced albuminuria, preserved in alcohol or other fixatives which 
coagulate albuminous material, this substance may be seen within Bow- 
man's capsule or in the lumina of the tubules as fine or coarse granules. 







f* ■" ' - 








i.si , 


■~: .J-- ' 


i$-- - 


'■■■W 


:.-$^. -, ■.. 








m^mf^ m&mm?^r: ■ ' ■ymp^ 






^0^ ■' ;i;^- '/ : ■ ,/;-##■ 



"^^^^m 



Fig. 326.— Hyaline Globules in Uriniferous Tubule. 
There is also degeneration and disintegration of the epithelium. 

Albuminous material in the tubules may form casts (see below) or when 
the conditions are favorable fibrillar fibrin may form. 

Casts. — Albuminous material which under various abnormal condi- 
tions has escaped from the blood-vessels in solution may coagulate, 
especially in the lumina of the tubules, forming the more or less cylin- 
drical or globular structures called casts. These may be homogeneous 
in structure^hyaline casts ; or the albuminous material of which they 



THE uiii:n^aky organs. 567 

are formed may be mingled ^ith the products of degeneration and disin- 
tegration of epithelial cells, either from the glomeruli or from the tubules ; 
or with red blood cells, or leucocytes, or exfoliated epithelial cells. In 
this way granular casts, epithelial casts, blood casts, etc. , are formed. The 
epithelium of the tubules may peel off in masses, forming cast-like cell 
structures. Homogeneous globules of various sizes may be formed in 
the tubular epithelium which is yet in place, and as the cells degenerate 






S 






.^ 






■:■ .;%\ 


-'■^ 




' / 








\> -^ ;■ 






■-'« 




-. 




-"-~;.%v 


^■^iif^'>;-, \ 


■"^<r 




I'pl 


-,:..i^.J 


j^ ■>■. 


^'"^ 


W^ 



m 



Fig. 327.— Hyaline Casts in Uriniferous Tubule. 
The epitbelium is flattened in the tubules containing the casts. 

and disintegrate, such homogeneous globules may collect in the lumina 
of the tubules (Fig. 326) or they may fuse to form hyaline casts (Fig. 
327). Homogeneous casts giving the micro -chemical characters of amy- 
loid are of occasional occurrence in the tubules. 

Casts and cell detritus may form both in the cortical and medullary 
tubules and may pass out of the organ with the urine. 



DEGENERATION. 

Albuminous Degeneration (Parenchymatous Degeneration — Acute Degen- 
eration). — This form of degeneration is most common in the acute infec- 
tious diseases, such as dii)htheria, scarlatina, measles, typhoid fever, yel- 
low fever, and in many forms of septicsemia and toxaemia. It usually 
accompanies similar lesions in other viscera. In moderate degrees of 
the lesion, the epithelium, particularly of the convoluted tubules, is 
swollen and more coarsely granular than normal (Fig. 328). In more 
pronounced lesions in addition to simple albuminous degeneration the 
epithelium may become more or less filled with minute fat droplets, or 
the cells may disintegrate and peel off, or they may become necrotic and 
the nuclei fail to stain. The cell body may then undergo coagulation or 
disintegrate. 



568 



THE UEIXAEY ORGANS. 



The gross appearance of the kidneys varies with the degree and ex- 
tent of the degeneration. The kidney may be slightly or considerably 
enlarged. On section the cortex is usually thickened and pale with ob- 







Fig. 328.— Albuminous Degeneration of the Kidney (Acute Parenchymatous Degeneration) . 

From a case of yellow fever, a. The swollen and granular epithelium peeling off and disintegrating ; b. 
hyaline material in the lumen of the tubule. 

literation of the normal cortical markings. The capsule of the kidney 
is not abnormally adherent. WTien there are other associated or an- 
tecedent lesions in the kidney, the gross appearance of the organ varies. 
Fatty Degeneration. — This may occur in those diseases of the blood or 
circulatory system in which general nutrition suffers ; in infectious dis- 
eases often associated with or following albuminous degeneration; in 






fi^® 









'-^^"L^ :''h^j^^^ 



^^* 



Fig. 329.— Fatty Degeneration of the Epithelium in the Convoluted Tubules of the Kidney. 
The fat droplets are stained hlack by osmic acid. 



THE URINARY ORGANS. 



569 



various cachexise ; in acute and chrouic forms of kidney disease, and in 
poisoning by phosphorus, arsenic, etc. 

The degeneration may be diffuse and widespread or it may occur in 
patches. If diffuse, the cortex in which it is most marked is usually 
more or less thickened, opaque, and yellowish ; if in i)atches, there are 
opaque yellow streaks or spots in the cortex. But these appearances are 
often obscured by various other lesions. If the degeneration be moder- 
ate in degree, there are larger and smaller fat droplets, usuallj^ most 
abundant in the basal portion of the epithelium of the convoluted tubules 
(Fig. 329). In more marked degeneration, the cells of the convoluted 




Fig. 330.— Amyloid Degenkration oe Tuft Capillaries in the Kidney. 

a, The tuft is completely transformed into a waxy mass ; l», portions of tuft waxy ; c, tuft capillaries nor- 
mal ; d, convoluted tubule with disintegrating- epithelium. 



tubules may be filled with fat droplets and may peel off, or they may 
disintegrate, setting the fat free in the lumen of the tubules. The de- 
generation may involve the tuft and capsule epithelium as well as that 
of the collecting tubes, and fat droplets may be found free or in cells in 
the interstitial tissue. 

Amyloid Deg-eneration, — This is usually associated with amyloid de- 
generation elsewhere in the body and commonly occurs in kidneys which 
are already the seat of various forms of chronic lesion. Usually the 
kidney is enlarged, the section is shining or translucent, the cortex is 
thick and pale, the glomeruli are often unusually plain. The capillaries 
of the tufts (Fig. 330) and the vasa recta are most often involved. If the 
kidney be otherwise altered, the gross and'microscopic appearances vary. 

Glycogen Degeneration of the epithelium may take place in diabetes 



570 THE URINARY ORGANS. 

inellitus. It is usually most marked in the cells of Henle's loops (Fig. 
331). 

Calcification may occur in chronic inflammatory lesions or in old in- 
farctions ; in the intertubular tissue of the medulla in the aged, or in 
casts in the collecting tubes. 

INFLAMMATION. 

General Considerations. 

Many of tlie alterations in the kidney which are commonly considered inflammatory 
are in fact degenerative, and these degenerative changes are often so important and so 
conspicuous in the lesions as to fairly dominate the gross and microscopic appearances. 
The processes in the kidneys which may be properly considered inflammatory are either 
exudative or productive, so that the apparently complex series of kidney changes which 
are grouped under the name nephritis, or Bright's disease, are really phases of exudative 
or productive inflammation, or both, associated with degenerative processes. 

Whether the kidneys be large or small, white or red or mottled, smooth or rough; 
whether the disease be acute or chronic, it is always these comparativley simple proc- 







Fig. 331.— Glycogen Degeneration op the Epithelium op the Kidney in Diabetes. 

esses, varying in extent, in duration, in intensity, and in relative predominance, which 
are to be taken into the account in the study of inflammation of this organ. 

There are perhaps no lesions whose classification has seemed beset with such difii- 
culties as those of the kidneys. This is largely due to a failure to realize that the vari- 
ous phases of inflammation and degeneration do not stand apart as independent proc- 
esses or lesions, but are closely associated and often merge. It is difficult, perhaps 
impossible, to make a classification which shall meet the requirements of the clinic, 
the limitations of urinary tests, and at the same time accord with the revelations of the 
autopsy and the microscope. 

One of the difficulties in framing a classification of kidney lesions is that there are 
many and serious abnormalities in the function of the kidney which do not find expres- 
sion in such structural changes as we can at present recognize. Our knowledge of such 
of the minute structural lesions in the renal epithelium as are not manifested by altera- 
tions in the size and form and organic integrity of the cell is, in fact, very meagre. 
So that the attempt to classify inflammatory lesions of the kidney upon both clinical 
and morphological data often leads to conjecture or confusion, frequently to both. 
Considering the scope of this book and our present purpose, it seems wiser to set forth 
here as concisely as possible the essential character of the lesions in acute and in chronic 
phases of inflammation and degeneration in the kidney based upon morphological rather 
than upon clinical data. 

It is convenient to divide the acute inflammatory processes of the 
kidneys into two forms, Suppurative Nephritis and Acute Diffuse Nepliritis. 



THE URINARY ORGANS. 571 



Suppurative Nephritis. 

Suppurative inflammation of the kidney may follow injury with local 
infection. It is, however, most often due to the presence of bacteria, 
commonly the pyogenic cocci, which have been brought through the 
blood-vessels from a remote infective focus, as in ulcerative endocarditis, 
septic phlebitis, etc. — embolic infection. Or, on the other hand, the bac- 
terial excitant may be transmitted to the kidneys through the urinary 
passages — ascending infection. 

Traumatic lesions of the kidney may lead to suppurative nephritis 
either through direct infection of the wound or by the establishment of 
local vulnerability (see footnote, page 160) to the action of bacteria which 
may later gain access to the injured tissue through the circulation. 
After infected wounds or injuries of the kidney, large abscesses may 
develop, or nearly the whole organ may be converted into a mass of pus, 
blood, and disintegrated tissue. 

In the embolic ty])e of suppurative nephritis, small abscesses are formed 
most frequently in the cortex. Where bacteria lodge and grow in the 
tissue there is at first circumscribed hypersemia or hgemorrhage and 
necrosis, with subsequent gathering of leucocytes and finally the disin- 
tegration of tissue and the formation of abscess. Such kidneys present 
to the naked eye on section small sj)ots — or in the medulla streaks — which 
are red or gray or yellow, depending upon the degree of advancement of 
the lesion. In such areas the bacteria may be readily demonstrated, 
sometimes in early stages in dense masses in the capillaries and other 
smaller vessels, or later scattered through the necrotic and disintegrat- 
ing tissue (Fig. 91, page 182). Embolic abscesses are commonly devel- 
oped in both kidneys and by extensive coalescence may give rise to large 
abscesses. There is reason to believe that in certain forms of septicaemia 
bacteria may secure a foothold in the tubules, not as emboli, but through 
excretion. In such cases the suppurative foci may be at first limited to 
the medulla. 

Ascending Infection. — In suppurative nephritis associated with a sim- 
ilar process in the ureter, bladder, etc. , the medullary portion of the kid- 
ney is usually earliest involved and then the elongated form of the suppur- 
ative areas corresponds to the grouping of the tubules in this region. ' 

\Vhatever the form in which it may manifest itself, suppurative in- 
flammation of the kidney is commonly induced by some one or combina- 
tion of the pyogenic micro-organisms which may lodge within it under 
favorable conditions. Thus Streptococcus pyogenes. Staphylococcus 
pyogenes, Bacillus coli communis. Bacillus pyocyaneus. Bacillus proteus ; 
the pneumococcus, the typhoid bacillus, and others, may be found in the 
suppurative foci. Sometimes, however, especially in the more chronic 
processes, micro-organisms are not demonstrable. 

^ For further details concerning suppurative nephritis consecutive to similar proc- 
esses in adjacent organs see below. 



572 THE URINA_RY ORGANS. 



Acute Diffuse Nephritis. 



This process may occur in acute infectious diseases ; it is especially 
common in scarlatina and not infrequent in diphtheria, typhoid fever, the 
exanthemata, malaria, and in septicaemia due to various bacterial ex- 
citants. 

The lesions of acute diffuse nephritis vary greatly in extent, in degree, 
in the relative involvement of one or other renal structure, as well as 
with the duration of the process. In this as in other forms of inflamma- 
tion of the kidney, degeneration is an important and often predominant 
factor in the morphology of the lesions. 

We shall now consider those lesions which in varying degrees are 
characteristic of an early phase of acute diffuse nephritis, such as fre- 
quently occurs in the course of the acute infectious diseases. While 
changes in the different structural components of the kidney may occur 



"l 








ST 




*'\ 


?i 










.^^^ 


0, 



Fig. 333.— Acute Diffuse Nephritis. 
Showing swelling of the cells covering the capillary tufts and lioing Bowman's capsule. 

simultaneously and are intimately related to each other, we shall study 
first the lesions of the gJomeridi, second those of the tubules, third those 
of the interstitial tissue and its vessels. 

The Glomeruli. — One of the early alterations in the tufts of the glom- 
eruli is the swelling of the cells which cover the capillaries. ^ These cells 
which in normal conditions are thin and scarcely visible, save by their 
nuclei, now project from the capillary loops, sometimes remaining closely 
apposed to the capillary walls, sometimes assuming polypoid shapes 
(Fig. 332), sometimes forming a continuous thick covering of cuboidal 
cells over the vessels. The nuclei are larger than normal and mitosis 
may be evident. Similar changes occur in the epithelium between the 
capillary loops. The capillaries are sometimes distended and plugged 
with cells ; some of these are leucocytes ; others are larger with large 
nuclei and may be swollen endothelium. Hyaline thrombi are often 
found in these tuft capillaries. The swollen and proliferating tuft epi- 
thelia often undergo fatty degeneration and may peel off into the glom- 
erular space. 

^ For a study of the development of the glomeruli and its relation to pathological 
changes see Eerring, Jour. Path, and Bact., vol. vi., p. 459, 1900. 



THE UJm^ARY ORGANS. 573 

In some cases the iDroliferation and exfoliation are extensive and 
the cells may collect in crescentic masses within Bowman's capsule, 
crowding the tuft toward its hilus. The cells in these crescentic masses 
may be flattened from pressure and in profile appear fusiform (Fig. 
333). The capsular epithelium may be swollen or remain apparently 
intact while there is a large cell accumulation from the tuft ; or it may pro- 
liferate or become fatty or peel off. Swelling, exfoliation, and prolifer- 
ation of the glomerular epithelium in some degree are of frequent occur- 
rence in acute nephritis. They are sometimes so pronounced, especially 
in acute nephritis following scarlatina, either with or without extensive 
associated lesions as to have suggested a name for one phase of the lesion 
— glomerulo -nephritis. There is sometimes a considerable accumulation 
















Fig. 333.— Acute Diffuse Nephritis— following Scarlatina. 

Swollen cells are seen upon the capillary tuft and lining Bowman's capsule. Polyhedral and flattened 
cells lie in masses between the capsule and the tuft ; the latter has been pressed upon by the cells and 
other exudate within the capsule. 

of albuminous exudate between the tuft and capsule. Such albuminous 
material in specimens fixed by alcohol is in the form of fine granules and 
may be mingled with exfoliated and often fatty epithelium or cell detritus. 

Leucocytes and red blood cells may be ]3resent with other exudate 
within Bowman's capsule. 

Tl\e Tuhides. — The lesions of the tubules of the kidney in the early 
phases of acute nephritis are largely degenerative ; the epithelium, es- 
pecially of the convoluted tubules, is swollen and coarsely granular (Fig. 
328), or it may contain few or many fat droplets (Fig. 329) ^albuminous 
and fatty degeneration. The epithelium may become necrotic and may 
disintegrate or peel off over larger or smaller areas. Thus the lumina of 
the tubules may contain fragments of epithelium or detritus mingled with 
albuminous fluid — serum — red blood cells and leucocytes, or hyaline or 
other forms of casts (Fig. 327). Eed blood cells may be extravasated 
in considerable numbers and collect in the tubules or pass on with the 



574 



THE UEINARY ORGAISTS. 



exudates. The casts and other exudates may be preseut iu the cortex or 
in the collecting tubes of the kidney. 

The Interstitial Tissue. — This in early phases of acute nephritis may 
be oedematous or it may be more or less infiltrated with leucocytes or 
fibrinous exudate. Patches of new-formed small spheroidal cells, or 
larger cells with conspicuous excentric nuclei may be present either in 
the vicinity of the glomeruli (Fig. 334) or near the interlobular veins, 
or a general thickening of the interstitial tissue may occur even very 




Fig. 334.— Acute Diffuse Nephritis. 

Showing proliferation of cells on the tuft and lining the capsule of the glomerulus and the formation of new 
interstitial tissue with large polyhedral cells— glomerular and interstitial type. 



early in some forms of acute diffuse nephritis, particularly in those fol- 
lowing scarlatina and diphtheria. 

We have thus seen that in the early phases of an acute inflammation 
of the kidneys, such as may occur independently or in connection with 
acute infective processes elsewhere, there is an involvement of all the 
structural units of the organ, the glomeruli, the tubular epithelium, and 
the interstitial tissue. Such a process involving the various kinds of 
tissue is called diffuse, ' and the process is therefore designated Acute Dif- 
fuse Nephritis. 

^ It should be understood that the word " diffuse " is not used in the sense of wide- 
spread or uniform, but as indicating involvement of the various structural units of the 
organ. 



THE URIXARY OEGA^^S. 575 

While both kidneys are involved in acute diffuse nephritis, the lesions 
in each are hj no means uniform either in extent or advancement and 
are often patchy or irregular in distribution. 

Variations in Type in Acute Diffuse Nephritis. — There are many varia- 
tions in the type of the lesions in acute diffuse nei)hritis, some of which 
seem to be directly dependent upon the character of the excitant, while 
in others the variations cannot as yet be associated with known determin- 
ing conditions. 

If one guard himself against the notion of distinct species in the le- 
sions it is convenient to recognize certain structural variants or types. 
Thus the changes in the glomerular capillaries and epithelium may, 
as above indicated, be prominent — glomerular tyjye— (so-called glomerulo- 
nephritis) (Figs. 333 and 334) ; the degenerative process in the tubular 
epithelium may be extreme — parenchymatous or degenerative type ; there 









^%m 






Fig. 335.— acute Diffuse Nephritis. 

Showing pus cells and granular exudate in the tubules, with flattening of the epithelium ; also moderate 
oedema of the interstitial tissue— exudative type. 

may with other lesions be considerable haemorrhage into the glomeruli 
tubules and interstitial iissue—hwrnorrhagic type. With or without marked 
structural invoh^ement of the parenchyma and interstitial tissue there 
may be an exudative inflammation in which serum and leucocytes (Fig. 
335) and more or less red blood cells may gather in the glomeruli or tu- 
bules and with various forms of casts pass off in the urine. This, which 
is common, has been called by Delafield the exudative type of acute diffuse 
nephritis. Finally, with any one or more of the above types of lesion 
there may be early and significant involvement of interstitial tissue of 
the kidney, so that new and often very cellular tissue, either in small 
patches or through a large portion of the organs, may lead to tubular 
atrophy and to serious and permanent structural alterations. This, which 
has been called by Delafield the productive type, by others the interstitial 
type of acute diffuse nephritis (Fig. 334 and 336), is most frequent as a 
complication of scarlatina ; it may follow diphtheria, or puerperal infec- 
tions, and may occur as an apparently independent process. ' 

'Consult for an interesting study of "acute interstitial nephritis," Councilman, 
Jour. Exp. Med., vol. iii., p. 393, 1898' Councilman regards the new cells in the inter- 
stitial tissue as largely " plasma cells " derived from lymphoid cells of the blood. 



576 



THE URINARY ORGANS. 



Between these types of lesion, largely based, as will be seen, upon the 
relative involvement of the structural units of the kidney, are many in- 
termediate forms which the scope of this book does not permit us to 
consider. 

Kidneys which are the seat of acute diffuse nephritis sometimes ap- 
pear almost normal on gross inspection. But in more typical forms they 




Fig, 336.— Acute Diffuse Nephritis. 

A vertical section of the cortex, showing the -vvedge-shaped growth of connective tissue with atrophy of 
the glomeruli and tubules in the region especially involved, which is the territory of one of the interlobular 
arteries. This is acute nephritis of the productive type. 



are slightly or considerably enlarged, the capsule is free, the cortex is 
thickened, and either reddened or pale or mottled red and gray. When 
the interstitial tissue is oedematous the cortex may appear translucent. 
The glomeruli may be red or pale and conspicuous or normal in appear- 
ance. The pyramids may seem unusually red by contrast with the 
thickened iDale cortex. In hsemorrhagic forms of acute nephritis in 
which blood may collect in the glomeruli in the interstitial tissue and in 
the tubules, the cortex may be mottled with red. 

In many forms of acute diffuse nephritis, particularly if the inter- 
stitial tissue be not considerably involved, resolution may take place. 

The Excitants of Acute Diffuse Nephritis. — In many cases of acute dif- 
fuse nephritis, the process seems to be due to toxic substances which are 
formed under the influence of micro-organisms in other parts of the body 
and presumably excreted by the kidney with whose cells they come into 
intimate contact or in whose metabolism they may share. Acute nephritis 



THE URINARY ORGANS. 



577 



is also induced by various exogenous poisons, such as corrosive subli- 
mate, carbolic acid, cantharides, and many others; it may occur with 
extensive lesions of the skin and after exposure to cold. In the acute 
nephritis following extensive burns, exposure to cold, etc. , it is probable 
that the poisonous products of abnormal body-cell metabolism are the 
direct excitants. 

Bacteria may be eliminated from the body through the kidney some- 
times without inducing lesions which are demonstrable with our present 
technique. ' The following bacteria have been found by numerous ob- 
servers in the kidney and in the urine, in acute diffuse nephritis : the 
typhoid bacillus, pneumococcus, streptococcus and staphylococcus, the 
colon bacillus, and others. The Plasmodium malarise may be present in 
the kidney in large numbers.^ To what extent the kidney lesions are due 
to the presence of these organisms themselves and to what extent to elimi- 
nated toxins is not yet clear. 

Persistent and Advancing- Lesions following Acute Diffuse Nephritis. 

If we follow the alterations which the kidney in acute diffuse nephritis may un- 
dergo, if resolution do not occur, but the process continues, we find that in each of the 







^i*.; W.:-:'7:^:'^mm^m, 







Fig. 337.— Diffuse Nephritis. 

Showing an advancing lesion following an acute type. Note the formation of a patch of dense fibrous tis- 
sue, with thickening of the walls of the glomeruli and atrophy of the tubules. 



three structural units of the kidney, the glomeruli, the tubules, and the interstitial tissue 
with the blood-vessels, important changes take place which often lead to slight or to 

^See BiecU and Kraiis, Arch. f. Exp. Path. u. Phar., Bd. xxxvii., p. 1, 1896, bibli- 
ography; also V. Klecki, ibid., Bd. xxxix., p. 178, 1897; ^Iso Sittmann, Deut. Arch. f. 
klin. Med., Bd. liii., p. 323, 1894. 

-For a study of malarial nephritis, see TJiayer, Am. Jour. Med. Sciences, vol. cxvi., 
p. 560, 1898. 

See for the study of a case of acute malarial nephritis with large numbers of para- 
sites in the kidney, Evnng, Trans Assn. Am. Phys., vol. xvi., 1901. 
37 




578 THE URINARY ORGANS, 

marked deformities of the organ, and to such minute changes as are in fact charac- 
teristic of what we are wont to call chronic diffuse nephritis. 

The capillaries of the tufts may become partly or wholly obliterated by a gradual 
thickening of their walls and an increase of the connective tissue between them, wiiile 
at the same time Bowman's capsule is thickened and contracts upon the altered tuft 
(Fig. 337) with which it may unite so that the glomerulus may finally be represented 
by a small, dense spheroidal mass of fibrous tissue (Fig. 338). 

The interstitial tissue of the kidney may be increased in patches, most often at first 
near the glomeruli or along the interlobular veins. This tissue may at first be quite 
cellular, resembling a collection of small spheroidal cells or larger polyhedral cells, 
among which new fibrillar stroma may develop ; or there may be a more diffuse in- 
crease of connective -tissue cells and stroma. As this new-formed fibrous tissue grows 
less cellular it contracts, the tubules which it encloses are atrophied, the epithelium 

may undergo fatty degeneration and peel off or become 
flattened, casts may be present in the narrowed lumen 
and the tubules may at last be represented by a small 
cluster of flattened cells without distinct tubular structure, 
or they may disappear altogether (Fig. 337). Such islets 
or masses of new-formed fibrous tissue enclosing variously 
altered and atrophied remnants of glomeruli and tubules 
vary greatly in size and usually merge gradually into less 
altered kidney tissue. When they are formed near the 
|L« ^H '*'<^^My'-l\', ^ surface of the kidney, the shrinkage of the fibrous tissue, 

>3 '^'^^'^^'^ " - > r which is continuous with the inner layers of the capsule, 

V ^ >K *-^. ^^^ draw the surface inward, leaving between the irregu- 

lar depressions the areas of less altered, or otherwise al- 
FiG. 338.— Atrophied Glom- tered, kidney tissue somewhat projecting in irregular 
ERULus IN CHRONIC Nephri- kuobs or grauulcs. Thus arise the granular surface and 
'^^^' the adhesion of the capsule which are frequent in some 

The tuft is converted into a forms of persistent diffuse nephritis, 
dense mass of fibrous tissue. ^^ ^j^^ ^^^^^ ^f ^^^ j^.^^^^^ j^^g involved, or not at all 

involved in the production of new fibrous tissue, the tu- 
bules may undergo marked alterations. Thus the epithelium may be swollen and 
coarsely granular or fatty ; it may become necrotic so that the nucleus fails to stain; 
it may, when necrotic or degenerated, peel off or disintegrate so that the tubules may 
be extensively denuded. On the other hand, the epithelium may remain in position 
but be much thinner than normal, while the lumen is largely dilated. This maj^ take 
place by the blocking of the tubules below by desquamated cells or by compression 
of new-formed interstitial tissue. The whole tubule, not merely the lumen, may be di- 
lated and irregular in shape, with well-preserved or fatty or otherwise altered epithe- 
lium. Casts of various forms may be present. 



Chronic Diffuse ^Rephritis. 

General Considerations. — We have seen that when the inflammatory 
process in the kidneys, at first acute, is protracted, both the degenerative 
and the productive lesions may become more marked and extensive. 
Thus with a preponderance now of the interstitial alterations and again 
of the degenerative or other changes in the parenchyma, the kidneys in 
a condition of chronic diffuse nephritis may present a considerable va- 
riety in gross as well as microscopical appearance. They are sometimes 
larger than normal, as is often though not always the case when the par- 
enchyma is more conspicuously involved ; or smaller, as is usual when 
the interstitial lesions are widespread or advanced. 



THE URIXAEY OEGAXS. 579 

Although there is no sharp line of separation, either clinical or mor- 
phological, to be drawn between acute and chronic diffuse nephritis, it 
is convenient to group kidney lesions in this way with the understanding 
that many intermediate forms exist, as must be the case, since, as we 
have seen, acute nephritis may pass gradually into the chronic form. 

^ATiile acute diffuse nephritis may be followed by the alterations 
which have just been summarized and which are characteristic of certain 
phases of chronic diffuse nephritis, the latter process, it should be remem- 
bered, is by no means always or usually preceded by an acute form of in- 
flammation. 

In some phases of chronic diffuse nephritis, although interstitial 
alterations are present, the lesions of the tubules may be the most prom- 
inent feature ; thus albuminous and fatty degeneration, disintegration, 
flattening and peeling of the epithelium, the formation of casts, the dila- 
tation of the tubules, etc. , may be most conspicuous. In another mor- 
phological group of kidneys in chronic diffuse nephritis, while there are 
many alterations in the tubules, the most marked change is the increase 
in amount and the subsecpient contraction of the interstitial fibrous tissue 
with atrophy of the tubules and glomeruli and the consequent diminu- 
tion in size and alteration in shape and consistence of the organ. Be- 
tween these extremes of lesion there are all intermediate forms, in 
kidneys which are larger than normal, of normal size, or smaller than 
normal. 

In endeavoring to classify or group the lesions in chronic diffuse 
nephritis, one encounters difficulties similar to those which beset a like 
attempt in the acute forms of renal inflammation. But the difficulties are 
enhanced in the former case by the fact that the conditions under which 
the lesions develop are far more diverse and variable and at the same 
time are often much more obscure. 

If we leave out of sight for the moment the conditions under which 
chronic diffuse nephritis may arise and the direct excitants which with 
more or less certainty can be fixed upon as important and confine our 
attention to moriDhology, it is at least convenient to place in one group 
as above indicated kidneys in which, while there may be important 
changes in the glomeruli and in the interstitial tissue, the most marked 
lesions are in the tubular epitlielium. This may conveniently be called the 
parenchymatous or degenerative tyjje of chronic diffuse ne2)hritis. 

On the other hand, there is another large and important class of kid- 
neys which are characterized morj)hologically by a relatively prominent 
increase in the amount of interstitial fibrous tissue with associated destruc- 
tion by atrophy or otherwise of the tubular structures. This may be 
called the interstitial type of chronic diffuse nephritis. 

In considering this in many respects artificial grouping of persistent 
inflammatory kidney lesions, it should be i^membered that while the 
parenchymatous and the interstitial tyx)es of lesion may originate as such 
and so persist, the lesion of the parenchymatous type may, as the disease 
progresses, assume the characters of the interstitial form. 



580 THE URINARY ORGANS. 

Parenchymatous Type of Chronic Diffuse Nephritis. — This may originate 
in an acute diffuse nephritis but more frequently develops independently 
of this. As in other forms of diffuse nephritis, the tubules, the glom- 
eruli, and the interstitial tissue are more or less invclved. The lesions 
are most marked in the cortex (Fig. 339), and here the epithelium may 




Fig. 339.— Chronic Diffuse Nephritis— Parenchymatous Type. 

At the left is a band of new-formed fibrous tissue with atrophy of tubules and swelling and prolifera- 
tion of the capsule cells ; in the central portions the tubular epithelium is disintegrating at the edges, while 
at the right the lumina of the tubules are dilated, with flattening of the epithelium. 

be swollen and coarsely granular or is often fatty. Droplets of clear 
fluid may form within the epithelium — so-called ^^ vacuoles. '^ The epi- 
thelium may be flattened or it may peel off or disintegrate and the ceils 
and cell detritus together with leucocytes, red blood cells, and casts may 
collect in the irregular and often widened lumina. The casts may be 
hyaline or granular or epithelial, or they may be covered with leucocytes 
or red blood cells. In the glomeruli, the tuft and capsule cells may 
swell and proliferate and peel off (Fig. 340) ; albuminous fluid which in 
specimens hardened in alcohol is represented by a granular precipitate 
may be present in the intracapsular space and in the tubules. The in- 
terstitial tissue may be increased in amount, usually in circumscribed re- 
gions, and here the enclosed tubules are atrophied, ^ot infrequently, 
more or less extensive haemorrhages occur. 

If the disease have been of long standing the new-formed interstitial 
tissue may be present in considerable amount with much destruction of 
the tubules. The glomeruli may be compromised by the thickening of 
Bowman's capsule and the obliteration of the capillaries, so that at length 
the tuft and capsule may fuse and the glomeruli may be represented by 



THE URINARY ORGANS. 



581 



deuse fibrous nodules (Fig. 338). The growth of interstitial tissue in 
patches may, when near the surface of the organ, bind the capsule to the 
kidney so that in its removal small masses of the parenchyma may be 
stripped off, leaving a rough surface on which grayish depressed areas, 
corresponding to the interstitial growth, are intermingled with more pro- 
jecting light or yellowish portions, in which albuminous or fatty degen- 
eration of the tubular epithelium may be marked and extensive. Yery 
often the new fibrous tissue develops along the course of the interlobular 
vessels so that cylindrical or narrow, wedge-shaped areas are affected, ex- 
tending inward from the capsule (Fig. 341). Amyloid degeneration in- 
volving the capillary tufts, the vasa recta, and the larger arterial trunk 
is common. 

Such kidneys as have just been described present varying gross ap- 
pearances which are dependent u.pon the character, extent, and distribu- 













Fig. 340.— Chronic Diffuse Nephritis. 

Showing swelling of tuft and capsule epithelium : flattening of the tubular epithelium and slight increase 

in the interstitial tissue. 



tion of the lesions. Some are larger than normal with a thickened whit- 
ish or yellowish cortex. These are often called large ichite kidneys. But 
kidneys with essentially similar lesions are not always large, are often 
nearly normal in ai:>pearance, or may be smaller and with a cortex thinner 
than normal. If haemorrhage into the tubules or interstitial tissue be a 



582 



THE URINARY ORGANS. 



3^ 









.•t.^-^X'5^ 



(5?4S 















•2?' 






-^ 



,1^-:- 



■^r* -?' . 












marked feature of the lesion, the cortex may be reddish or mottled red 
and yellow. Such are the so-called large 7^ed Mdneys. 

Arterio- sclerosis and cardiac hypertrophy frequently accompany this 
type of kidney lesion. 

Interstitial Type of Chronic Diffuse Nephritis. — The type of chronic dif- 
fuse nephritis in which the growth of interstitial tissue is conspicuous, 
which may be called the interstitial or indurative type, apparently some- 
times represents a later phase of the parenchymatous type ; or it may re- 
sult from chronic congestion, or be associated with arterio-sclerosis ; but 

it appears to be more fre- 
|^;^^^Vt^-^£^ - :^' -^ c - '^'^^t^^ h:;^;^ quently an independent proc- 
ess. As the new interstitial 
tissue which is formed in 
patches or streaks or large 
masses gradually becomes less 
cellular, more dense, and 
shrinks, the kidneys are 
usually smaller than normal 
and, owing to the uneven dis- 
tribution of the lesion, rough 
upon the surface when the 
thickened and adherent cap- 
sule is stripped off. The 
areas of the cortex in which 
the fibrous tissue is most 
abundant (Fig. 342) are 
grayish or translucent and de- 
pressed, while the parenchy- 
ma between, often fatty, pro- 
jects as yellowish rounded 
knobs or granules. This con- 
dition is therefore sometimes 
spoken of as ^'granular atro- 
phy,'^ and such kidneys are 
often called ^^ granular kid- 
neys ^^ or ^^ atrophied kid- 
neys. ^' The tissue is firm and 
resistant to the knife ; and on section the cortex is seen to be in general 
thinned, often extremely so, some portions being much more atrophied 
than others. Cysts of various sizes may be formed from dilatation and 
coalescence of tubules. The cortex is usually more involved than the 
medulla. The fat with which the kidney is surrounded is often largely 
increased. 

On microscopical examination the new-formed interstitial tissue is 
sometimes in patches (Fig. 343) or streaks along the course of the in- 
terlobular vessels, with less affected regions between them. In these 
fibrous portions there may be flattening of the epithelium and various de- 



m. 







Fig. 341. 



-Chronic Diffuse Nephritis— Parenchyma- 
tous Type. 



Showing a wedge-shaped mass of new-formed tissue ex- 
tending inward from the capsule of the kidney, to which it 
is firmly attached. The tubules within the fibrous area are 
atrophied, while the tubules elsewhere show various degen- 
erative epithelial changes. 



THE URIXAEY ORGANS. 583 

grees of atrophy or complete destruction of the epithelium and the tu- 
bules. Between these fibrous regions, little altered tubules may be pres- 
ent or those with granular and fatty degeneration, exfoliation, and dis- 
integration of the epithelium. Various forms of casts may be present in 
the tubules ; the epithelium may be flattened with enlargement of the 
lumen. The glomeruli are variously altered ; thus there may be thicken- 
ing of the capillary walls and of Bowman's capsule (Fig. 344), increase 
and exfoliation of the tuft and capsular epithelium, or a more or less 
complete conversion of the glomerulus into a knob of dense fibrous tissue. 









■^>.}^;^^ 



Fig. 342.— Chronic Diffuse Nephritis— Atrophied Kidney. 

The capsule is thickened and adherent, especially to the dense mass of fibrous tissue at the left of the 
section in which the tubules are greatly atrophied. At the right the parenchyma is less atrophied, but here 
the lumina of the tubules are dilated, the epithelium is degenerating and flattened. 

In advanced phases of the lesion the kidney may be very small ; then 
a large part of the tissue is involved ; and while the atrophy is always 
more marked in some places than in others, it is often difficult to find 
any normal structural elements. 

Fibrous thickening of the walls of the arteries and veins of the kid- 
neys is usual in this type of chronic diffuse nephritis (Fig. 345). 
Amyloid degeneration of the vessels is not infrequent. The heart is 
often greatly hypertrophied and general arterio- sclerosis is common. 

Variations in Type in Chronic Diffuse Nephritis. — There are many vari- 
ants in the two types of chronic diffuse nephritis which we have briefly 
described. It is possible to indicate in a general way morphological 
appearances which are frequently present and more or less character- 
istic of each of the variants when the kidney lesions occur in connection 



584 



THE URINARY ORGANS. 



with either gout or chronic visceral cougestiou or arterio -sclerosis or 
syphilis. But these variations in form cannot be further considered here. 




Fig. 343.— Chronic Diffuse Nephritis. 

Showing interstitial tissue, dense and fibrous in type, between the tubules. The epithelium is in part flat- 
tened ; in places shows albuminous degeneration. 

The diverse appearances which the kidneys present in chronic diffuse 
nephritis are, as we have seen, largely due to variations in local and gen- 
eral tissue vulnerability or to the rapidity and to the stage of develop- 




■m. 



'J 






Fig. 344.— chronic Diffuse Nephritis. 



Showing fibrous thickening of the glomerular tuft with a inass of dense fibrous interstitial tissue at one side 
(below) of the glomerulus. From an atrophied kidney. 



THE UEIXAEY OEGAXS. 585 

ment of the lesions as well as to the nature of the excitants. But acute 
inflammatory processes not infrequently sui^ervene in kidneys which are 
the seat of slowly developed chronic processes ; so that lesions tyi^ical of 
both acute and chronic nephritis are not infrequently associated. Finally 
it is evident that the grouiDing of the kidneys in chronic diffuse nephritis 
in accordance with the structural elements of the organ most conspicu- 
ously involved is essentially artificial, since this in many cases is simply 
an indication of the period of the disease at which the patient died. 

The Excitants of Chronic Diffuse Nephritis. — The conditions under which 
chronic diffuse nephritis occurs are most diverse. Thus, judging from 
the clinical history, it may be a primary process ; it may follow infec- 
tious diseases either with or without a previous acute nephritis ; it is not 
infrequently associated with gout and syphilis, with lead poisoning, with 
excessive use of alcohol, with arterio-sclerosis, with general chronic con- 
gestion of the viscera, with chronic 

sui)purative and tuberculous processes, ^ji^^yj^'^- f-^\^- 

and appears in many cases to develop ,.>*S^^- ~--^'^->t^v^ 

under the influence of dietetic excesses /^/^' -^^ ' _- ^ \^ 

and protracted gastro -intestinal dis- " // ' . ' ^ ^^ ""x^, v,^ 

orders. The ' nature of the excitants 'r \ f , v_:_i^ ^ i-^- 
under these various conditions is most ■ // i > ^ ■ J "^^ ^ \'>: 

obscure. Although in gout, lead poison- -/; , ^ ^^^ — ^'K''f. ' f J *>" 
ing, alcoholism, etc., a fairly definite ' 1' \ ^ ^ :^ -'^_^ ' ^ / ; ' 
inciting toxic agency may be assumed, V-^ ^^^^v-^ --' /" j ^ yf 

the exact mode of action of such ex- 4:Vr,"^ ^-- ^ -' '^;:^'^ 

trinsic or intrinsic poisons is almost ^^'^-<.^^.:T, .,• -'v'^r v' 

wholly unknown. In regard to other ^-^ - - ^ 

excitants of chronic diffuse nephritis, ^^*^- ^^^--chronic obliteratixg end- 

■■- ' ARTERITIS IX AX ATROPHIED KiDXEY 

the prevalent views as to the impor- with chroxic diffuse nephritis. 
tance of disturbed metabolism in the 

body which may lead to the excretion of abnormal harmful products 
favor the conjecture that in many cases at least both the degenerative 
and the productive processes may be the marks of a persistent auto- 
intoxication. 

The relationship between arterio-sclerosis and chronic kidney lesions 
is not clear. Nor is it certain, assuming the initial importance of ob- 
structive vascular lesions, whether the new formation of fibrous tissue 
should be regarded as a primary productive inflammation or as replace- 
ment hyperplasia secondary to ei^ithelial degeneration and tubular 
atrophy. 

It should be remembered that in most cases the lesions of chronic 
diffuse nephritis are not independent, but are usually associated with 
those of other viscera. The significance of this association varies greatly. 
AVhile the kidnej' lesions may be primary they are very often secondary 
to other visceral abnormalities, or the whole series of lesions may be de- 
pendent upon a common known or unknown etiological factor. 



586 THE URINARY ORGANS. 



Tuberculous :N^ephritis. 

Miliary tubercles may be present in the kidney in general acute mili- 
ary tuberculosis or in a localized tuberculous inflammation which is most 
marked elsewhere. Eenal tuberculosis is, however, most often associated 
with tuberculous processes in other parts of the genito -urinary tract. It 




Fig. 346.— Tuberculous Nephritis. 

is not infrequently primary in the kidney and then is often unilateral. If 
only one kidney be involved the other may become the seat of chronic 
diffuse nephritis with waxy degeneration of the walls of the arteries. 
Tuberculous inflammation may occur in a kidney already the seat of 
chronic inflammatory changes. 

The process is apt to begin in the mucous membrane of the pelvis and 
calyces, and extends from thence first to the pyramidal and afterward to 
the cortical portion of the kidney. In the mucous membrane of the 
pelvis and calyces there is a growth of new cellular tissue studded with 
tubercle granula ; w^hile the epithelial cells proliferate, become deformed, 
and desquamate. This process is often soon followed by cheesy degen- 
eration of the inflammatory products. Similar changes occur in the 
kidney which may become extensively involved and largely destroyed. 
The portions of the organ which do not share directly in the tuberculous 
process often develop lesions of the interstitial type of chronic diffuse 
nephritis or of suppuration. Thus the kidney may become hollowed out 
into a series of ragged cavities with caseous and disintegrating walls 
(Fig. 346). 

Sometimes the process comes to a standstill, and then the caseous por- 
tions may be infiltrated with salts of lime. 



THE URINARY ORGANS. 587 



Syphilitic Inflammation. 



Giimmata of the kidney are of occasional occurrence. A close rela- 
tionship between syphilitic arteritis and atrophied forms of chronic dif- 
fuse nephritis seems probable. ' 

SUPPURATIVE PYELITIS AND PYELO-NEPHRITIS. 

Suppurative Pyelitis is often associated with suj)puration of the kid- 
ney substance, more frequently, with a similar process in the bladder or 
ureters. But it may occur by itself. It is incited by the same micro- 
organisms as are concerned in the induction of the associated lesions in 
the kidney and bladder ; in the latter case, it is most often the Bacillus 
coli communis, the Streptococcus pyogenes, and Staphylococcus pyogenes. 

The mucous membrane of the pelvis may be congested, thicker and 
more opaque than normal, and coated with pus or with patches of fibrin. 
The presence of pelvic calculi is to be regarded as a predisposing rather 
than as a direct inciting agent in sui^purative pyelitis. 

Suppurative Ureteritis. — The conditions under which suppurative in- 
flammation of the ureter occurs are similar, as is the general appearance 
of its mucous membrane, to those just indicated in the pelvis. 




Fig. 347.— Chronic Pyelo-Nephritis. 
Showing dilatation of the pelvis and calyces. 

Suppurative Pyelo-Nephritis with Cystitis. — In this association of lesions 
of the bladder and kidneys, which is usually initiated by the inflamma- 
tion of the bladder, the affection of the kidneys is commonly bilateral. 
The suppurative areas in the kidney may be in the form of small ab- 
scesses scattered through the kidneys, or in the form of elongated whitish 
streaks or wedges between the tubules. The purulent foci are often sur- 
rounded by a red zone of congestion. 

^For bibliography see Delamare, Gaz. d. Hopitaux, May 12tli, 1900. 



588 THE URINARY OEGAl^S-, 

The kidney tissue in the vicinity of the abscesses may be necrotic, the 
outlines of the cells being iDreserved but their nuclei absent or not I'e- 
vealed by the usual staining agents. 

The infective agent may traverse the ureters in passing from the 
inflamed bladder to the kidneys, leaving the mucous membrane of the 
ureter intact. 

Chronic Pyelo-Nephritis. — Chronic cystitis or calculi in the pelvis of 
the kidneys may set ui3 a chronic inflammation which involves both the 
pelvis and calyces and the kidney tissue. The mucous membrane of the 
pelvis and calyces is thickened, the epithelial layer is changed, there is 
a growth of granulation tissue beneath the epithelium, and there may be 
little polypoid outgrowths. The surface of the mucous membrane is 
coated with pus or fibrin, or the cavity of the pelvis and calyces are di- 
lated and distended with purulent serum (Fig. 347). 

The kidney itself is the seat of a chronic interstitial inflammation 
with the production of new connective tissue, and sometimes of pus, with 
obliteration of the renal tubules. 

HYDRONEPHROSIS. 

Dilatation of the pelvis and calyces of the kidneys may be congenital 
and may be associated with other malformations. The pelves and caly- 
ces of both kidneys, and the ureters, are distended with urine ; the blad- 
der may be also distended and its wall hypertrophied. The urethra may 
be closed, or no obstruction can be demonstrated. 

In adults hydronephrosis may follow mechanical obstruction of the 
urethra or ureters, from inflammation, tumors, or calculi. According 
to the iDOsition of the obstruction, either one or both kidneys are in- 
volved. 

The pelvis and calyces are dilated, sometimes enormously, and filled 
with urine alone or urine mixed with pus. The kidney tissue is flat- 
tened and thinned over the distended cavities. Its texture may remain 
unchanged, or there may be developed suppurative pyelonephritis or 
chronic diffuse nephritis. 

PERINEPHRITIC SUPPURATION". 

The loose connective tissue about the kidney may become the seat of 
suppurative inflammation. This may follow mechanical injury or may 
be secondary to suppurative or other inflammatory xDrocesses, such as 
caries of the spine, empyema, pelvic cellulitis, puerperal parametritis, 
perityphlitis, and suppurative nephritis. It may be associated with 
acute infectious diseases in children. The suppuration may extend back- 
ward through the muscles ; downward into the iliac fossa, the perineum, 
the bladder, the scrotum, or the vagina ; forward into the peritoneal cav- 
ity or the colon; or upward through the diaphragm. 

The kidney itself may be simply compressed by the abscess or be- 
come involved in the suppurative process. 



THE UEINARY ORGANS. 



589 






CYSTS IN THE KIDNEYS. 

Cysts are formed iu the kidneys both during intra-nterine and extra- 
uterine life. 

Cong-enital Cystic Kidneys are often striking objects. Either one or 
both kidneys may be greatly enlarged and converted into a mass of cysts 
(Fig. 348). The cysts are of various sizes and are separated from each 
other by fibrous septa or compressed kidney tissue. They may contain 
a clear yellow, acid fluid hold- 
ing in solution the urinary 
salts; or the fluid is turbid 
and brown, and contains blood, 
uric-acid crystals, and choles- 
terin. The cysts are often 
lined with a single layer of flat, 
polygonal cells. Some of them 
seem to be formed by a dilata- 
tion of the tubules and of the 
capsules of the Malpighian 
bodies. As causes for such 
dilatations there may be found 
obliteration of the tubes in the 
papilla?, and stenosis of the 
pelvis, ureters, bladder, or ure- 
thra. Other congenital mal- 
formations are often associated 
with this. 

Cysts of the Kidney in the 
Adult may be single and occur 
in otherwise normal organs. 
There may be one or more 
cysts filled with clear or brown 
serum or gelatinous material. 
These cysts do not appear to 
interfere with the function of 
the kidneys. 

In chronic diffuse nephritis, 
especially in the atrophic form, groups of tubes may be dilated. Ap- 
parently one or more of the larger tubes in the pyramids is obstructed, 
and this causes dilatation of a corresponding group of tubes. Such a dila- 
tation may be moderate in size, or it may form cysts visible to the naked 
eye. Occasionally both kidneys are very much enlarged and converted 
into a mass of cysts containing clear or colored serum or gelatinous ma- 
terial. The nature of these cysts is uncertain : they may be congenital. 
They are sometimes associated with similar cysts in the liver. ' 

^ For a study of cystic kidney with extensive bibliography see Ritchie, Labora- 
tory Reports, Royal College of Physicians, Edinburgh, vol. iv. 




Fig. 348.— CONGENiTAi. Cystic Kjdney. 

Only very small portions of the kidney tissue remain, 
crowded between the cysts. 



590 THE URINARY OEaANS. 



RENAL CALCULI. 

In the kidneys of new-born cliilclren, from the first to the fourteenth 
day after birth, the large tubes of the i3yraniids often contain small, 
brownish, rounded bodies composed of the urates of ammonium and so- 
dium. Similar masses may also be present in the calyces and pelves. 
In still-born children these masses are usually absent. The carbonate 
and phosphate of lime may be deposited in the tubes of the pyramids, in 
the form of white linear masses, in the kidneys of old persons and of 
those who have suffered from destructive diseases of the bones. 

Urate of soda in the form of acicular crystals is deposited both in the 
tubes and stroma of the kidneys of gouty persons. 

Concretions of the urinary salts are often formed in the pelves of the 
kidneys. They may remain there as rounded masses, or they may attain 
a large size and be moulded into the shape of the pelvis and calyces. 
Smaller calculi may pass into the ureter and either become impacted 
there or pass through it into the bladder. The most common form of 
calculus is that composed of uric acid. But they may also be formed of 
uric acid with a shell of oxalate of linie, or of oxalate of lime alone, or 
of the phosphates, or of cystin. 

The most serious result of the presence of these calculi is the occlu- 
sion of the ureters or the incitement of pyelo-nephritis. 

TUMORS. 

Small fibromata, lipomata/ myomata, and angiomata may occur in the 
kidney and with the exception of the fibromata are most common in the 
cortical portion. Papilloma may form in the mucous membrane of the 

pelvis. Sarcoma, myxosarcoma, and 
endothelioma, often of large size, 
may develop in the kidney. These 
tumors are frequently soft and vas- 
cular and are prone to hsemorrhage. 
Primary sarcoma of the kidney is 
s. -. 'i'^tvl^vJ t^i''#V>!*'^V'^^''^ common in children. Secondary 







-■^- SJ,- 






sarcoma of the kidney is not rare. 
Adenoma is of frequent occur- 

^;;^%^M ' , , ^ rence in the kidneys. It usually 



- - ».->. ^. ^ z ,F--?,,s .H:l;"^f>'l r'-^ I 5 originates in the cortex and may be 

'yi'' '?''"^'^"^^^"^^^^^ ' ^ invisible, or not larger than a pea 

;^^ >J?i< '-^f/ ' -H'^^ ^ ^. (Fig. 349) or it may invade the me 

^>--»«?^-^-"'l'" '/"^.--^/'O' '. '>><i.. I'i . dulla or lars^elv rei:)lace the kidnev 



% 



^j^--V^s^^'^-Nv'-^^' '^^ '0.^,^%# ^ dulla or largely replace the kidney. 
.^"'^ . '^^"/"-C*-/ "'"7^--^'^ The adenomata are usually light in 

"^^ '^'^^^'"■^^ "'. , "'* ' ^^ T^. ^^ ^ See for studies and bibliography of 

lipoma UlricJi, Zie tier's Beitr. z. path. 

FIG. 340.-SMALL ADENOMA OF THE KiDxXEY. ^^^^ ^ g^ ^^^^:^ ^ ^Qg ^^^^ . ^^^^ ^^y^^,,^ 

Situated in the cortex. Virchow's Arch., Bd. cxlv., p. 339, 1896. 



THE UEINAHY ORGANS. 591 

color save when very vascular with haemorrhage, and they may be sepa- 
rated from the kidney structure by a fibrous capsule. Such tumors are 
not rare in children. ' 

There are two principal varieties of these tumors, the papillary and 
the alveolar, which are, however, closely related. 

1. FcqnUary Adenoma. — There are cavities of different sizes, from the 
walls of which spring branching tufts covered with cylindrical or cuboi- 
dal epithelium (Fig. 350). These tufts nearly fill the cavities. 

2. Alveolar Adenoma. — There is a connective-tissue framework en- 
closing small round, oval, or tubular alveoli, lined or filled with cells 




Fig. 350.— Adenoma of the Kidney. 
Papillary variety. 

(Fig. 351). The cells are usually large and may be cylindrical, cuboi- 
dal, or j)olyhedral, and may be pigmented in a manner similar to the 
cells of the adrenals. 

Fatty degeneration of the epithelium may be excessive and glycogen 
may form in the cells. In these tumors the stroma may be present in 
considerable quantity, or the blood-vessels may form conspicuous fea- 
tures, or a cystic distention of the alveoli may occur. Large areas in 
these tumors may become necrotic. Many of these tumors appear to 
have developed from adrenal cells astray in the kidneys. They jnay 
form metastases. 

The relationship between true adenoma of the kidney, adenomata 
which api^ear to develop from strayed adrenal elements, and similar 
^ See Engelken, Ziegler's Beitr., Bd. xxvi., p. 320, 1899, bibliography. 



592 THE URINARY ORGANS. 

tumors which are regarded by some observers as endotheliomata or endo- 
thelial sarcomata, and certain forms of angio-sarcoma, is not yet alto- 
gether clear/ 

Primary carcinoma of the kidney is rare, adenoma being frequently 
mistaken for it. Secondary carcinoma is not infrequent. 

PARASITES. 

Echinococcus, in its ordinary form of mother and daughter cysts, is 
sometimes found in the kidney. The cysts may open into the pelvis of 
the kidney, into the pleura, or through the wall of the abdomen. 




Fig. 351.— Adenoma of the Kidney. 
Alveolar variety. 

Cysticercus cellulosae is of very rare occurrence. Filaria sanguinis 
hominis is found in the arteries, veins, lymphatics, and stroma, and may 
pass into the urine. Strongylus gigas has been found several times in the 
pelvis of the kidney. 

The Urinary Bladder. 

Malformations. 

Absence op the Bladder is of rare occurrence. The bladder may be very small, 
the urine passing almost directly into the urethra. The bladder may be separated into 
an upper and a lower portion by a circular constriction. It may be completely divided 

^ For a careful study of tumors and other growths in the kidney see Kelynack, 
"Renal Growths," 1898, bibliographv ; also references to bibliography, Busse, Virchow's 
Arch., Bd. clvii., pp. 346, 377, 1898; also Kelly. Philadelphia Med. Jour., vol. ii., 1898, 
pp. 223, 283, bibliography; also Burkhardt, Deutsche Zeits. fiir. Chir., Bd. Iv,, p. 91. 
bibliography. 



THE URINARY ORGANS. 593 

b}^ a vertical septum into tAvo lateral portions. Diverticula of the wall of the bladder 
are sometimes found in new-born children. Partial or complete closure of the neck of 
the bladder ma}^ occur. This may lead to hj^dronephrosis, or the urine may be dis- 
charged through the open urachus. 

ExsTEOVERSiON of the bladder is one of the most frequent malformations, and may 
occur in either sex. It presents several varieties: 

1. The umbilicus is lower down than usual, the pubic bones are not united at the 
symphysis, the pelvis is wider and shallower than it should be. Between the umbilicus 
and pubes the abdominal wall is wanting. In its place is a projecting, ovoid mass of 
mucous membrane, in which may be seen the openings of the ureters. The penis is 
usually rudimentary ; the urethra is an open fissure (epispadias) ; the clitoris may be 
separated into two halves. The ureters usually open normally; sometimes their open- 
ings are displaced or are multiple. They may be dilated. 

2. There may be a fissure in the abdominal wall, filled up by the perfectly formed 
bladder. 

3. The umbilicus may be well formed, and there is a portion of abdominal wall 
between it and the exstrophied bladder. 

4. The external genitals and urethra may be well formed, and the symphj^sis pubis 
united, while only the bladder is fissured. 

5. The genitals, urethra, and symphysis may be Avell formed, the bladder closed 
except at the upper part of its anterior wall. The bladder is entirely or in part inverted 
and pushed through the opening in the abdominal wall. 

The Ukachus normally remains as a very small canal, 5 to 7 cm. long, with 
a small opening into the bladder, or entirely closed at that point. If there is a congen- 
ital obstruction to the flow of urine through the urethra, the urachus may remain open 
and the urine pass through it. Or the bladder may present, even in the adult, a slender 
distention reaching close to the umbilicus as the result of a persistent urachus. 



Changes in Size and Position. 

Dilatation. — This may be general or partial, leading to the formation of diver- 
ticula. 

General dilatation of the bladder is produced by the accumulation of urine in con- 
sequence of some mechanical obstacle to its escape, or of paralysis of the muscular 
walls of the organ. The dilatation is usually uniform and may be very great, so that 
the bladder may reach to the umbilicus. If the w^alls of the bladder are paralyzed, or 
the obstruction occm's suddenly or is complete, the wall of the bladder is thinned. 
When an incomplete obstruction exists for some time the Avails of the bladder are apt 
to hypertrophy, so that, although the bladder is larger than normal, the walls may not 
only be of the usual thickness, but e\en very much thicker. In the foetus dilatation of 
the bladder may reach such a size as to interfere with delivery. 

The retained urine in dilated bladders is liable to decomposition, from the presence 
of bacteria, and this may lead to inflammation or gangrene of the mucous membrane. 

DivERTicrLA of the bladder may be produced by the pouching out of circumscribed 
portions of the wall of the bladder, the Avail of tlie pouch containing all the layers of 
the bladder wall. More frequently, hoAvcA^er, they are produced by a protrusion of 
the mucous membrane between hypertrophied bundles of muscle fibre. They may be 
very small (Fig. 352), or they may be as large as a child's head. They may communi- 
cate with the bladder by a large or small opening. The decomposition of stagnant 
urine in diverticula is apt to induce inflammation. Calculi may be formed in them or 
may slip into them from the bladder. 

Htpertrophy of the muscular coat of the bladder is usually due to mechanical 
obstructions to the outfloAV of urine, such as stricture of the ruTthra, enlarged prostate, 
calculi, new growths, etc. The muscular coat is thickened uniformly or assumes a tra- 
beculated appearance. The organ retains its normal capacity, or is dilated, or becomes 
smaller. The mucous membrane is frequently the seat of chronic or acute inflamma- 
38 



594 THE URINARY ORGANS. 

tion. Dilatation of the ureters and hydronephrosis frequently accompany this con- 
dition. 

Hernia of the bladder sometimes accompany intestinal hernise through the ingui- 
nal and crural canals and the foramen ovale. The changes in position of the bladder, 
produced by displacements of the vagina and uterus, will be mentioned with the lesions 
of those organs. 

In the female the base of the bladder may press downward, causing protrusion of 
the vaginal wall {vaginal cystoceU); or there may be inversion and prolapse of bladder 
through the dilated urethra. 



WOUNDS— RUPTURE— PERFORATION. 

Penetrating wounds of the bladder may permit escape of urine into 
the abdominal cavity, or infiltration into the surrounding connective 




Fig. 352.— Diverticula of the Bladder. 

tissue, or permanent fistulge. Such wounds are always serious and fre- 
quently fatal, owing chiefly to the severe and often gangrenous inflam- 
mation which decomposing urine sets up in the connective tissue, or to 
the peritonitis induced by the same cause. 

Bupture of the bladder may be produced by severe blows and falls 
when the bladder contains urine. More rarely rupture takes place from 
overdistention. Death may occur from rupture of the bladder with 
escape of urine into the peritoneal cavity, without evidences of perito- 
nitis. 

Ferfo7xitions of the bladder may be due to ulceration and gangrene, 
to abscesses from without, and to cancerous ulceration from the adjoin- 
ing organs. Fractures of the pelvic bones may be accompanied by lacera- 
tion of the bladder. Perforations of the bladder may lead to the estab- 
lishment of fistulse, communicating with the rectum, vagina, uterus, or 
opening externally. 



THE UEINAKY ORGAKS. 595 



DISTURBANCES OF CIRCULATION. 

Hyper 8emia. — Aside from active hypersemia of the mucous membrane 
in acute inflammation, the bladder is not infrequently the seat of chronic 
congestion from obstruction to the venous circulation. Under these con- 
ditions there may be chronic catarrhal inflammation, or a marked dilata- 
tion of the veins (vesical haemorrhoids), which may give rise to haemor- 
rhage or to obstruction of the opening of the ureters. 

Haemorrhage. — Extensive hemorrhages into the bladder are commonly 
due to injury or to the presence of calculi or tumors. Small haemor- 
rhages into the substance of the mucous membrane may accompany in- 
flammation, the haemorrhagic diathesis, scurvy, purpura, smallpox, etc. 
If the haemorrhage is considerable and occurs rapidly in an empty blad- 
der, a clot is apt to form ; but when the blood mixes with urine as it is 
extravasated it more commonly remains liquid and is discharged as a 
reddish-brown fluid. 

INFLAMMATION. (Cystitis.) 

Acute Catarrhal and Exudative Cystitis. — This may be incited by the 
presence of urine which has decomposed under the influence of bacteria ; 
by cantharides or other drugs ; by the presence of foreign bodies and 
calculi ; or it may be due to an extension of gonorrhoeal urethritis or va- 
ginitis ; or it may occur with acute general infectious diseases. The 
mucous membrane is swollen and congested, although these alterations 
may not be very evident after death. There may be ecchymosis : the 
epithelium is granular and may proliferate and peel ofl". Leucocytes 
may infiltrate the submucosa and pass out between the epithelial cells. 
Mixed with the urine there may be shreds of mucus, pus cells, epithelial 
cells of various shapes, usually more or less swollen and granular, or 
fragments of such cells ; red blood cells, bacteria, and various urinary 
crystals ; abscess may form in the mucous membrane ; or there may be 
phlegmonous inflammation in the submucosa and muscularis of the bladder 
with formation of abscesses. Thus perforations and fistulae may occur. 
Eesolution may take place after acute catarrhal and exudative cystitis, 
but it very frequently assumes a chronic character. 

Chronic Cystitis. — In this form the mucous membrane may be swollen, 
succulent, grayish, or mottled with spots of congestion or extravasation, 
and covered with a layer of mucus and pus. Microscopically the mem- 
brane may be more or less infiltrated with pus cells, and pus may be 
constantly produced and thrown off into the urine. Later the mucous 
membrane may become thickened either diffusely or in the form of tufts 
or polypi. In some cases it becomes atrophied. Owing to decompo- 
sition of the haemoglobin in the extravasated blood the mucosa may 
become pigmented, brown, or slate -colored. The mucous membrane fre- 
quently becomes eroded, especially on the most elevated portions, or 



596 THE URINARY ORGANS. 

deep ulcerations may occur. The muscular coats may become paralyzed 
and the bladder dilated ; or the submucosa or the muscularis, or both, 
may become hypertrophied. The mucous membrane may become en- 
crusted with urinary salts. 

In another class of cases the inflammation assumes a necrotic charac- 
ter. Larger and smaller shreds and i^atches of the mucosa die, become 
brown or gray in color, loosen or peel off, and become mixed with the 
urine and exudations. The gangrenous process may extend to all the 
coats of the bladder, so that perforation and fatal peritonitis may occur. 
The gangrenous form of cystitis is more apt to occur in paralytics. 

In still another class of cases the inflammation is suppurative. The 
submucosa, the intermuscular connective tissue, and the adjacent parts 
become infiltrated with pus, either diffusely or in the form of larger and 
smaller abscesses, which may open externally or internally, forming deej) 
ulcers. In all these cases the inflammation may extend to the ureters 
and kidneys ; it may skip the ureters and involve the kidneys. 

The small nodules of lymphoid tissue in the mucous membrane of 
the bladder, especially near the neck, may become enlarged and promi- 
nent in cystitis, and may then be mistaken for miliary tubercles (nodular 
cystitis). 

Croupous Cystitis. — In connection with any of the above lesions the 
mucous membrane of the bladder may be covered, in patches or some- 
times over a considerable i)ortion of its surface, with a layer of fibrin, 
either granular or fibrillar, enclosing pus and epithelial cells and bac- 
teria. The mucosa may be infiltrated with fibrin. 

This form of inflammation may occur in connection with severe in- 
fectious diseases — measles, diphtheria, scarlatina, typhoid fever ; in con- 
nection with similar inflammation of the external genitals, in puerperal 
fever, noma, and sometimes in the presence of foreign bodies. It rarely 
occurs independently. 

In the so-called emphysematous cystitis, due to the presence of Bacillus 
aerogenes capsulatus, larger and smaller gas blebs may be present in the 
mucosa and underlying tissue.^ 

The most common micro-organisms which act as excitants of acute 
catarrhal and exudative cystitis are Bacillus coli communis. Streptococ- 
cus pyogenes, and Staphylococcus pyogenes, the gonococcus and typhoid 
bacillus,^ Bacillus proteus, and Bacillus aerogenes capsulatus. Many 
other forms are of occasional occurrence. 

Tuberculous Cystitis. — There may at first be miliary tubercles formed 
in the submucosa. By the coalescence of these and the degeneration of 
tissue about them, ulcers are formed, and it is most frequently in the 
ulcerative stage that the lesion is seen. The ulcers, which may be large 
or small, are usually most abundant at the base of the organ. Their 
edges may be cheesy, and miliary tubercles in greater or smaller num- 
bers are usually found in the mucosa about them. 'Not infrequently 

'See for Uhliogrsi])!! J Keclroicskt/, Centralbl. f. Path., October IStli, 1898, p. 817. 
^See Cursclwiann, Miinchener med. Wochenschr. , October 16th, 1900, bibliography. 



THE UEIXAEY OEGAXS. 597 

large shreds of tissue are loosened and cast off. The mucosa about the 
ulcers is apt to be infiltrated with small spheroidal cells. Tubercle ba- 
cilli are present in many of the tubercles and in the edges and base of 
the ulcers, and may be found in the urine. Catarrhal inflammation is 
a very constant accompaniment of this lesion. Tuberculous cystitis may 
occur in connection with tuberculous inflammation of the lungs, intes- 
tines, or of the kidney, uterus, prostate, etc. 

TUMORS. 

Small nodular fibromata may form in the submucosa. 

Aside from the polypoid thickenings of the mucosa occurring in 
chronic cystitis, soft vascular papillomata are of frequent occurrence. 
These tumors vary in size from that of a pea to that of a pigeon's egg or 



,^^ 






'---''^-^^- ^' 



Fi(t. 358.— Papilloma Of the Bladder. 



larger. They consist of a fibrous, often very vascular stroma, and are 
covered on the surface with numerous small, closely set, villous projec- 
tions, over which are irregular layers of elongated or cylindrical cells 
(Fig. 353). These tumors are very liable to bleed, are often accompanied 
by vesical catarrh, and may be covered by a precipitate of urinary salts. 
The epithelium is liable to peel off from the surface of the villi and ap- 
pear in the urine. Sarcoma of the bladder has been described. 

Carcinoma. — Carcinoma of the bladder is most frequently secondary, 
and is then rarely due to metastasis, but to an extension of the growth 
from neighboring parts, as the uterus, vagina, or rectum. 

Primary carcinoma of the bladder may occur : 

1. As a diffuse scirrhous infiltration of the entire wall of the bladder, 
usuallv with ulcerations of its inner surface. 



598 THE UEIN^ARY ORGANS. 

2. As a circumscribed nodule which grows inward and outward, ulcer- 
ating on its inner surface, and sometimes producing perforations. 

3. As a villous or pajnUomatous groivth. The tumor grows from one or 
more points of the inner surface of the bladder. It is formed of tubular 
follicles lined with cylindrical epithelium, while on its surface are tufts 
covered with cylindrical epithelium. The new growth may involve the 
entire thickness of the wall of the bladder. 

4. A few cases of carcinoma have been described in which the stroma 
contained a varying quantity of smooth muscle tissue. 

Cysts. — Dermoid cysts of the wall of the bladder have been described, 
but are rare. Small cysts with serous contents sometimes occur in the 
mucous membrane ; a part of them, at least, are believed to be due to 
faulty embryonal development. 

PARASITES, FOREIGN BODIES, AND CALCULI. 

Among the animal parasites occasionally found in the bladder may 
be mentioned Echinococcus, Distoma haematobium, Filaria sanguinis, Ascar- 
ides, and Oxyurides. 

A great A^ariety of foreign bodies may be found in the bladder, par- 
ticularly in the female. If their stay is long they are apt to become 
encrusted with urinary salts. 

Calculi. 

Vesical calculi may occur singly or in great numbers, and vary greatly in size, 
ranging from small, sand-like particles up to masses four or five inches in diameter, but 
the usual range is from the size of a pea to that of a hen's egg. They are usually oval, 
spheroidal, or elongated; or, when several are present, they are apt to be faceted. The 
surface may be smooth or rough. They are usually more or less distinctly lamellated, 
and are frequently formed around a central body called a nucleus, which may either be 
formed of urinary salts or some foreign body. Their most common constituents are 
phosphates, uric acid, and urates, and calcium oxalate, or various combinations of these. 

Uric- Acid Calculi. — These are the most common of vesical calculi. In the form 
of small brownish-red, crystalline aggregations they may be passed as "gravel." The 
larger uric-acid calculi are not commonly of very great size, are frequently finely nodu- 
lated on the surface, but may be smooth. The color varies from light yellow to dark 
reddish-brown; they are usually dense and lamellated. 

Calculi formed of Urates. — Calculi composed of pure urates are rare, these 
salts being more commonly combined with uric acid and the phosphates to form the 
complex calculi. Sodium urate, in the form of small spined, more or less globular 
crystalline masses, forms one of the varieties of " gravel. " 

Phosphatic Calculi. — Pure calcium-phosphate calculi are rarely found as whitish, 
usually smooth, and small lamellated concretions. 

Mixed or Triple Phosphate calculi are common, and frequently attain large 
size. These calculi are sometimes pure, but the deposit is more frequently associated 
with other salts, either as encrusting or intercalated lamellae. Triple-phosphate calculi 
are usually rough on the surface, of grayish-white color, lamellated, and frequently 
very friable. 

Calcium-Carbonate Calculi. — Small gray or white, hard, and usually smooth 
calculi of pure calcium carbonate occur rarely. Calcium carbonate is sometimes passed 
as gravel in the form of minute spheroidal bodies, either singly or in clusters. 



THE URINAEY ORGANS. 599 

Calctum-Oxalate calculi (mulberry calculi) are comparatively common, either 
pure or in combination with uric acid or the phosphates. Calcium oxalate may occur 
in the form of very small, hard, smooth concretions, or as larger, heavy, hard, finely or 
coarsely nodulated brown or blackish lamellated masses. The nucleus or some of the 
lamellae, or both, are often composed of uric acid. 

Cystin Calculi are usually ovoidal in shape, of waxy consistence, of clear or 
brownish or greenish-yellow color, with mammillated surface and crystalline fracture. 
Cystin may be associated in a variety of ways with other calculi. 

Xanthin Calculi, which are very rare, are usually of moderate size, smooth, of a 
cinnamon or cinnabar-red color, lamellated, and oval or flattened in shape. 

Solid masses of fibrin and blood sometimes occur in the bladder, and maj^ exist as 
independent structures, or form nuclei for the deposit of urinary salts. 

For a detailed account of calculi, the conditions under which they form, modes of 
analysis, etc, we refer to special works on this subject. 



The Urethra. 

Malformations . 

Some of the malformations of the urethra are described with those of the penis. 

The urethra may be impervious or may open at the root of the penis. More com- 
monly there is partial obliteration or stricture of some part of the canal. The entire 
urethra may be dilated into a sac. 

There may be a canal on the dorsum of the penis, formed by the fusion of the sper- 
matic cords, and opening in the glans above the urethra. 

There may be two or more openings of the urethra. The canal may be dislocated 
so as to open in the inguinal region. 

A number of cases have been reported in which a valve in the urethra has led to 
hypertrophy of the bladder, dilatation of the ureters, and hydronephrosis. 

. Owing to its narrowness, greater length, and peculiar connections with the internal 
generative organs, the male urethra is much more liable to disease than the female. 



Changes in Size and Position. 

Dilatation of the urethra may be produced by strictures, or by calculi or other 
bodies fixed in its lumen. The dilatations are fusiform or sacculated in shape, and may 
reach the size of an orange or be even larger. 

Strictukes of the urethra are usually due to inflammation of its walls. 

The stricture may be temporary, and due to a diffuse inflammatory swelling of the 
mucous membrane, or by the raising of the relaxed membrane into a fold or pocket. 

Permanent strictures are produced by structural changes in the walls of the urethra. 

1. The mucous membrane and submucous tissue become thickened in inflammation 
or as the result of injury and the new-formed fibrous tissue which contracts and narrows 
the canal. 

2. Ulceration of the mucous membrane leaves cicatricial tissue, which contracts, 
and also produces adhesions and bands of fibrous tissue. 

3. There is fibrous induration of the corpus spongiosum and consequent constric- 
tion of the urethra. 

The most frequent position of strictures is at the junction of the membranous and 
spongy portions of the urethra, or close to this point. They also occur at the fossa 
navicularis and the meatus, but frequently in the prostatic portion. There may be one 
stricture or several. The consequences of stricture are dilatation of the urethra, the 
bladder, the ureters, and hydronephrosis ; inflammation and ulceration of the urethra 
behind tlie stricture, with perforation, infiltration of urine, or the formation of fistulse. 

The urethra may also be obstructed by folds of the mucous membrane; by muscular 



600 THE UEII^ARY ORGANS. 

valves at the neck of the bladder; by wounds; by polypi and swollen glands; by new 
growths; by changes in the prostate and perineum; by calculi, mucus, blood, and 
echinococci coming from the bladder; by foreign bodies introduced from without. 

Prolapse and inversion of the mucous membrane occur occasionally in young 
girls and women. There is a bluish-red swelling, from the size of a pea to that of a 
walnut, at the meatus. In the male invagination of the mucous membrane of the ure- 
thra has been seen after injuries of the perineum. 



WOUNDS- RUPTURE— PERFORATION. 

Wounds of the urethra are i)roduced in many ways, but most com- 
monly by catheters and bougies. The wounds may cicatrize, or there 
may be infiltration of urine or the formation of fistulse or false passages. 

Biqdures of the urethra are produced by severe contusions and by 
fracture of the pelvic bones. Extravasations of blood and urine, and 
gangrenous inflammation of the surrounding soft parts, are the ordinary 
results. 

Ulceration and perforation of the urethra may lead to the formation 
of fistulse, which open in various directions through the skin. 



INFLAMMATION. (Urethritis.) 

Catarrhal Urethritis may be due to the action of chemical irritants, and 
to the extension to the urethra of inflammation from other parts ; but its 
most frequent excitant is the gonococcus. In its acute form it involves 
either a portion or the whole of the urethra. The mucous membrane 
is red, swollen, and covered with muco-pus. The epithelium may be 
loosened or exfoliated ; pus cells are present in the submucosa between 
the epithelial cells. The gonococcus is present usually in considerable 
numbers in the exudate, both free and in the pus cells. It may pene- 
trate between the epithelial cells. 

Eesolution may follow acute gonorrhoeal urethritis. But the condi- 
tion may become chronic and then is often confined to the posterior por- 
tions of the urethra. Here the gonococcus may persist for a long time 
and may be mingled with the exudate, which is now less purulent and 
consists very largely of mucus which in thread-like forms may be passed 
with the urine. 

Chronic Inflammation of the urethra may exist for a long time with 
the production of a muco-purulent exudation, but without the occur- 
rence of marked structural lesions. In other cases it leads to ulceration, 
to fibrous induration of the wall of the canal, to induration and swelling 
of the mucous follicles, to polypoid thickenings of the mucous mem- 
brane. 

The inflammation may extend to the fibrous wall of the urethra, the 
corpora spongiosa and cavernosa. This may result in the formation of 
new connective tissue or of abscesses, especially near the fossa navicu- 
laris. There may be involvement of the bladder, the glands of Cowper, 



THE UEINAEY ORGANS. 601 

the prostate, the spermatic cord, and the testicles. The inguinal glands 
also may be swollen and inflamed, and the lymphatic vessels on the 
dorsum of the penis may be involved in the same process. 

Croupous Inflammation is sometimes seen in children. Fibrinous casts 
of a small or large portion of the canal may be formed. 

Tuberculous Inflammation occurs rarely in the mucous membrane of 
the urethra in connection with tuberculous inflammation of the bladder, 
prostate, or testicles. 

Syphilitic Ulcers may be situated at the meatus or as far back as the 
fossa navicularis. They are apt to produce strictures. 



TUMORS. 

Aside from the polypoid outgrowths from the mucous membrane of 
the urethra as the result of chronic inflammation, fibrous polyps may oc- 
cur congenitally, or polyps containing glandular structures or cysts 
rarely occur. Carcinoma may occur as a result of local extension from 
adjacent organs or metastasis from the bladder. 

Cysts may occur in the mucous membrane as a result of the dilatation 
of the mucous glands. Circumscribed masses of dilated veins occasion- 
ally occur in the urethra, forming the so-called urethral hsemorrhoids. 

The sinus pocularis may be dilated in children by the retention of its 
secretion, so as to form a mass which may obstruct the exit of urine 
and lead to hypertrophy of the bladder and dilatation of the ureters. 



CHAPTER X. 

THE REPRODUCTIVE ORGANS OF THE FEMALE. 

The Vulva. 

Malformations. 

The external genitals may be entirely absent or imperfectly developed. The 
fissure between the labia may be unformed, or the labia may grow together, with or 
without obstruction of the urethra. The clitoris and nymphse may be abnormally 
large, or the nymphae may be increased in number. The clitoris may be abnormally 
long; at the same time the vagina is narrow, the uterus small and undeveloped or 
malformed; the ovaries are small, sometimes situated in the labia ; the mammse small, and 
the body is of a masculine character. Such cases are sometimes called pseudo-hermaph- 
rodites. The clitoris may be perforated by the urethra or may be cleft and appar- 
ently double. 

The hymen is subject to various anomalies. It may be entirely absent. The open- 
ing may be very large or in unusual places ; there may be several openings ; the free 
edge may be beset with papillary projections; there may be no opening at all. 

HAEMORRHAGE, HYPERiEMIA, ETC. 

Haemorrhage may take place from wounds or ulcers of the vulva, but 
the most important form of haemorrhage is that which occurs in the con- 
nective tissue of the labia majora. This may occur during labor or re- 
sult from external injury. One of the labia may be much swollen and 
distended by the extra vasated blood. The blood may be gradually ab- 
sorbed, or it may decompose with suppuration or gangrene of the sur- 
rounding tissue. 

Varicose Veins in the labia are not infrequent. (Edema of the labia 
majora may occur in pregnancy or in labor. It frequently accompanies 
disturbances of the venous circulation, as in certain heart and lung dis- 
eases ; or it may occur in chronic diffuse nephritis or other wasting dis- 
eases ; or as a result of thrombosis or other disturbances of circulation in 
the uterine or perivaginal venous plexuses. The latter may be excessive, 
leading to the transudation of fluid through the skin, to the formation of 
vesicles, or superficial erosion, or even of gangrene. 

INFLAMMATION. (Vulvitis.) 

The skin, mucous membrane, connective tissue, and glands of the 
vulva may be the seat of inflammation. 

Acute Catarrhal Inflammation of the mucous membrane may be in- 
duced by a variety of substances, but is most frequently due to gonor- 



THE EEPEODUCTIYE ORGANS OF THE FEMALE. 603 

rhoeal infection. The mncous membrane is swollen and red and covered 
with a muco-purulent exudate. The labia may be swollen, the glands 
of Bartholin are liable to be involved, and abscesses of the labia may be 
developed. 

Chronic Catarrhal Inflammation may lead to superficial or deep ulcera- 
tion of the mucous membrane, or to i)aj)illary outgrowths, or to thicken- 
ing of the labia. SuiDpurative inflammation of the tissue of the labia 
may occur with a similar process in neighboring parts. Erysipelatous 
Inflammation of the skin of the vulva is frequent in young children. In 
adults it is less common. Inflammation of the vulvo-vaginal glands 
may be acute and lead to abscesses, or chronic and produce induration 
of the gland. 

Gangrene may follow erysipelatous inflammation, or occur after par- 
turition ; it may accompany severe exhausting and infectious diseases. 
It may follow bruises or other injuries. In some forms, such as those 
known as noma and hospital gangrene, the destruction of tissue proceeds 
with extreme rapidity. 

Croupous Inflammation may occur, with or without diphtheria and a 
similar lesion of the fauces or elsewhere, and is frequently associated 
with gangrene. 

Tuberculous Inflammation, usually with ulceration, occasionally occurs 
in the vulva. 

Syphilitic Inflammation and ulceration are of frequent occurrence on 
the vulva, particularly on the mucous surfaces, and may lead to consid- 
erable destruction of tissue and cicatricial contractions. 

In one form, the so-called mucous pat di, there is an infiltration of the 
papillary layers of the skin or mucous membrane with variously shaped 
cells and fluid, so that the tissue has a gelatinous appearance. In other 
cases there is an hypertrophy of the papillse, so that larger and smaller 
wart-like excrescences are formed. This is called the pointed condyloma. 

TUMORS. 

Fibroma, — Circumscribed fibrous tumors are found in the connective 
tissue of the labia, mons veneris, perineum, clitoris, and entrance to the 
vagina. They may attain a large size, and, attached only by a pedicle, 
may hang far down between the legs. The skin is usually movable over 
the surface of these tumors. 

Fibroma diffusum (elephantiasis). — This usually involves the clitoris 
or the labia, or both, and may extend to surrounding parts of the skin. 
It consists essentially of a diffuse hypertrophy of the skin and subcuta- 
neous tissue, with or without involvement of the papillae and epidermis. 
The surface may be smooth or rough. When the i^apillse and epidermis 
are much involved, larger and smaller cauliflower-like excrescences may 
cover the hypertrophied parts and the surface be very rough and scaly. 

Papillomata. — These growths consist of hypertrophied papillae covered 
with thick layers of epithelium. They vary in size from that of a pea to 



604 THE REPRODUCTIVE ORGANS OF THE FEMALE. 

that of an apple, and have a cauliflower appearance. Lipomata, fibro- 
myomata, and fibro-sarcomata are of occasional occurrence in the vulva. 
A few cases of melano-sarcoma are recorded. Chondroma of the clitoris 
has been described. Carcinoma of the vulva may be primary, usually in 
the form of epithelioma of the clitoris or labia, or it may be secondary to 
cancer of the uterus, vagina, etc. 

Cysts are found in the connective tissue of the labia majora and 
minora. They are from the size of a pea to that of a child's head. 
They may contain serum, colloid material, purulent or bloody fluid, or 
they may have the characters of dermoid cysts or atheroma cysts. Their 
origin is in many cases obscure. In some cases they are doubtless due 
to dilatation of lymph-vessels. Cysts may be formed by a stoppage and 
filling mth fluid of the canal of IS^uck, or by a dilatation of the ducts or 
acini of the vulvo-vaginal glands. 



The Vagina. 

Malformations. 

The vagina may be entirely absent, and the internal organs of generation also ab- 
sent or imperfectly developed. Either the upper or the lower portion of the canal may 
be absent while the remaining portion is present. 

The vagina may be closed by an imperforate hymen or by fibrous septa at any part 
of its canal. The canal may be abnormally small without being occluded. 

The vagina may be double, in connection with a double uterus ; or, while the uterus 
is normal, the vagina may be incompletely divided by a longitudinal septum. 



Changes in Size and Position. 

Dilatation of the vagina is produced by tumors, by the prolapsed uterus, and by 
the accumulation of blood and mucus behind constrictions or obliterations of the canal. 

Lengthening of the vagina is produced by any cause which draws the uterus up- 
ward. Narrowing occurs as a senile change; is produced by the pressure of tumors or 
may follow ulceration of the wall of the canal through cicatricial contraction. 

Prolapse of the vagina occurs independently, usually as a result of thickening 
or laxity of its walls, or in connection with prolapse of the uterus. It may occur soon 
after parturition. A larger or smaller portion of the canal is inverted and projects 
through the vulva. The entire circumference of the canal ma}' be inverted and pro- 
lapsed, or only the anterior or posterior wall. The prolapse, at first small, may after- 
ward gradually increase in size and drag down the uterus with it. In other cases pro- 
lapse of the uterus is primary, and the vagina is inverted by the descent of that organ ; 
or the body of the uterus may retain its normal position, while an hypertrophy and 
lengthening of the cervix alone drags down the vagina. 

Hernia Vesico-Vaginalis — Cystocele — may be either the cause or effect of a 
prolapse of the vagina and uterus. If the cystocele be the primary lesion, it begins as 
a small projection of the wall of the bladder into the anterior part of the vagina. As 
the urine accumulates in this sac it increases in size, projects through the vulva, draws 
down the vagina and the anterior lip of the cervix, and finally the entire uterus. If 
the cystocele be the secondary lesion, it is produced by the dragging down of the pos- 
terior wall of the bladder by the inverted vagina. 

Hernia Intestino- Vaginalis. — A portion of the intestines may become fixed in 
Douglas' cul-de-sac between the rectum and the uterus. This portion of intestine grad- 



THE EEPEODUCTIYE ORGANS OF THE FEMALE. 605 

ually becomes larger, pushes forward the posterior wall of the vaghia, Inverts and fills 
up that canal, and finally projects through the vulva. It may drag with it the poste- 
rior wall of the vagina and the uterus. 

Rectocele Vagixalis. — A sac is formed by the projection of the anterior wall of 
the rectum and the posterior w^all of the vagina. This lesion is of rare occurrence and 
does not reach a large size. 

When the vagina is prolapsed there is usually inflammation of the lining membrane 
or a thickening of the epidermis. 



WOUNDS— PERFORATIONS. 

Wounds of the vagina are made by penetrating instruments, by f or- 
ceins and other obstetrical weapons, by the foetus during delivery or may 
result from coitus. Such wounds may heal, or give rise to large h^nemor- 
rhages, or suppurate, and lead to abscesses in the surrounding tissue, or 
leave fistulous openings into the vagina or they may by cicatricial con- 
traction in healing lead to constriction or obliteration of its canal. 

Vesico-vaginal Fistulse are usually produced by injuries from instru- 
ments or from the foetus during delivery ; less frequently by ulceration 
of the vagina, bladder, or adjacent connective tissue, or by abscess in 
the surrounding parts. The fistulae form an opening between either the 
bladder or the urethra and the vagina. They allow the urine to pass 
into the vagina. Spontaneous cure does not take place. 

Eecto-vaginal Fistulse are formed in the same way as the last-men- 
tioned. They allow the passage of gas or fseces into the vagina. They 
sometimes heal spontaneously. 

INFLAMMATION. (Vaginitis.) 

Catarrhal Inflammation of the vaginal mucous membrane may be acute 
or chronic. It is most frequently induced by the gonococcus, but may be 
due to local irritation or accompany active infectious processes. It not 
infrequently occurs in the new-born. In the acute form the mucous 
membrane is swollen and frequently covered with a muco-purulent or a 
purulent exudation. In the chronic form the mucous membrane may be 
swollen, covered with a purulent exudation ; there may be an exfoliation 
of epithelium, shallow or deep erosions, or ulcers. 

Sometimes large shreds or membranes are cast off from the vagina 
which consist wholly of exfoliated, flat epithelium. ' lu other cases the 
mucous membrane is thickened, dense, and sometimes pigmented, or 
it may be roughened, covered with papillae, or it may be relaxed and 
prolapsed. 

Croupous Inflammation may occur after parturition, in dysentery, in 
typhus and typhoid fevers, diphtheria, scarlatina, measles, and other 
infectious diseases. The mucous membrane is swollen and covered with 
a grayish layer of fibrin and pus. The mucosa and submucosa may be 
infiltrated with fibrin and pus. The infiltrated portions of the mucosa 
1 Consult McFarlcmd, Proc. Philadelphia Path. Soc, March 1st, 1899. 



606 THE REPEODUCTIYE OKGANS OF THE FEMALE. 

and submucosa may die and become gangrenous, and thus deep and ex- 
tensive ulcers be formed. 

Suppurative Inflammation of the fibromuscular coat of the vagina may 
occur after injuries or in pregnant and puerperal women. Abscesses 
may be formed which penetrate into the labia or into the pelvic connec- 
tive tissue. In other cases the intense phlegmonous inflammation may 
lead to the death and casting- off of portions of the vaginal wall, or even 
of the entire wall. 

Gangrene of the vagina may occur as a result of croupous or intense 
suppurative or syphilitic inflammation, or from unknown causes. In 
the form of noma it may be very extensive and rapidly destructive. 

Tuberculous and Syphilitic Inflammation, usually leading to more or 
less extensive ulceration, may occur in any part of the vagina. Tuber- 
culous inflammation is usually secondary to tuberculosis of other parts. 
Syphilitic ulcers may heal, sometimes leaving marked cicatrices, and 
sometimes not. 

TUMORS. 

Fibroma, fibro-myoma, sarcoma, myoma laevicellulare, are of occasional 
occurrence in the vagina. Myoma striocellulare is of rare occurrence. 

Papillomata are of frequent occurrence as a result of chronic inflam- 
mation. Carcinoma of the vagina is usually secondary to cancer of the 
uterus. It may be primary as a circumscribed nodular tumor, or more 
frequently it occurs in a papillary and ulcerating form and often spreads 
to neighboring parts. 

Cysts. — These are not very common and may be small or as large as 
a hen's ^gg. They may be lined with flattened epithelium, and contain 
serous or viscid, dark-colored or transparent fluid. ^ 

PARASITES. 

Among the animal parasites Oxyuris and Trichomonas vaginalis are of oc- 
casional occurrence. Among the vegetable forms Oidium albicans and Lep- 
tothrix are occasionally seen, while various forms of bacteria are common. 
Staphylococcus and Streptococcus pyogenes have been found many times 
in the normal vagina. While these and other bacteria may be harmless 
in the normal vagina, should conditions favoring their growth or an in- 
crease in their virulence occur, as after delivery for example, serious 
infectious processes may follow. The role of the gonococcus as an ex- 
citant of catarrhal inflammation is well established. 

The Uterus. 

Congenital Malformations. 

The uterus, tubes, and vagina may be entirely absent, with or without absence of 
the external genitals. Or the uterus alone, or the upper part of the vagina also, may 
be absent. 

^Consult Stokes, Johns Kopkins Hospital Reports, vol. vii., p. 109, bibliography. 



THE REPRODUCTIVE ORGANS OF THE FEMALE. 607 

The uterus may be only rudimentary while the vagina is normal. It then appears 
as a flattened solid body with solid cornua. Or there are two cornua joined at their 
lower extremities so as to form a small double uterus. Or the uterus is represented by 
a small sac, which may or may not communicate with the vagina. Or there is a very 
small uterus, with thin muscular Avails and two large cornua. 

Only one of the cornua which should form the uterus may be developed while the 
other is arrested in its growth. The uterus Is then a long, cylindrical body, terminat- 
ing above in one tube. On the side where the other horn should have been developed 
there is no tube, or only a rudiment. Both ovaries are usually present. 

The two cornua may be fully developed, but their lower ends remain separated and 
form a double uterus. An entire separation into two distinct uteri and vaginae is rare. 
More frequently the uterus consists of one body, divided by a septum into two cavities. 
There are then two cervical portions of the uterus projecting into a single vagina, or 
each into a separate vagina. Or there is only a single cervix. The septum in the 
uterus may be complete or only partial. 

The uterus may be abnormal in size or be variously flexed ; the cervix may be solid 
or may be closed by the vaginal mucous membrane. Or the cervix may have an ab- 
normal form with a small opening or canal. 



Changes in Size. 

In the new-born infant the uterus is small, the body flattened, the cervix dispro- 
portionately large. During childhood the organ increases in size, but the body remains 
small in proportion to the cervix. At puberty the shape changes and the body becomes 
larger. 

At every menstruation the uterus is somewhat swollen and congested. After preg- 
nancy it does not return to its virgin size, but remains somewhat larger. In old age it 
gradually becomes smaller; its walls are harder and more fibrous. 

Abnormal Smallness of the uterus is sometimes found as an arrest of develop- 
ment. It may result, however, from chronic endometritis, from repeated pregnancies, 
from old age, or from chronic exhausting diseases. Its cavity may be smaller than 
normal, or distended with mucus. Large myomata sometimes induce atrophy of the 
uterine wall. Atrophy of the vaginal portion of the uterus is sometimes observed after 
repeated pregnancies. Narrowing and obliteration of the cavity of the uterus and of 
the cervix are usually produced by chronic inflammation. 

Enlargement of the Uterus may be due to too early development. It is ac- 
companied by abnormally early development of all the sexual organs and functions. 
The uterus may be enlarged in connection with heart disease, prolapse and abnormal 
flexions and versions, chronic inflammations, repeated pregnancies, myomata, and ac- 
cumulations of blood or mucus in the uterine cavity. Enlargement of the vaginal por- 
tion alone may occur. One or both lips of the cervix may be uniformly increased in 
size, or they may be lobulated. 

Dilatation of the uterus is produced by accumulations of blood, mucus, or pus in 
consequence of narrowing or obliteration of the cervix or vagina. The uterine walls 
may retain their normal thickness, be thickened or thinned. The most frequent posi- 
tion of the stenosis is the os internum. The retained contents after a time change in 
character, forming a thin, serous fluid — Tiydrometra — or they may be mixed with blood. 
The dilated uterus may be of enormous size. If both os internum and os externum 
are closed the cervical cavity may be also dilated and the uterus have an hour-glass 
shape; or the dilatation may be limited to the cervix. If the obstruction is not com- 
plete, the retained fluid may escape into the vagina and be followed by a fresh accumu- 
lation. If the obstruction be in the vagina, th*e uterus and vagina may form a large, 
flask-shaped body, and the line of demarcation between cervix and vagina be lost. 

Accumulation of menstrual blood in the cavity of the uterus — hcematometra—\s 
usually due to congenital stenosis of the cervix or vagina, and ma}^ be very great. If 
the fluid is not evacuated by surgical interference there may be either rupture or ulcer- 



608 THE EEPRODUCTIYE ORGANS OF THE FEMALE. 

ative perforation of the uterus. The blood may escape into the abdominal cavity, or 
be shut in by adhesions, or perforate into the bladder or intestines. Sometimes the 
blood passes into the Fallopian tubes, dilates them, and escapes through their abdom- 
inal ends. 

Changes in Position. 

The body of the uterus may become fixed in an abnormal position, while the situa- 
tion of the cervix is unchanged. 

Flexion. — The body may be bent forward — anteflexion, ; backward — retroflexion ; 
or sideways — lateral flexion. The flexion may be slight, or so great that the neck and 
body form an acute angle. Anteflexion is the most common variety, and that in which 
the flexion is greatest. Peritoneal adhesions, flaccidity of the uterine walls, particularly 
after delivery, atrophy of the walls, ovarian and other tumors, etc. , are the usual causes 
of flexion. 

Version of the uterus consists in an abnormal inclination of the long axis of the 
organ to that of the vagina. The uterus may be inclined backward, forward, or to one 
side. 

Retroversion is the most common. The fundus uteri is directed backward and 
downward, the cervix forward and upward. This condition is found in various de- 
grees; in the highest the fundus lies in Douglas' cul-de-sac with the cervix upward, 
so that the axis of the uterus is parallel to that of the vagina, but in a direction nearly 
opposite to the normal. Abnormal looseness of the uterine ligaments, abnormally large 
capacity of the pelvis, enlargement or tumors of the uterus, and pregnancy during the 
first four months, are some of the more common conditions under which this lesion 
occurs. 

Anteversion. — Inclination of the fundus forward and downward, and of the cervix 
backward and upward, is not common and seldom reaches a high degree. It occurs 
under the same general external conditions as anteflexion. 

Lateroversion is not very common as a simple lesion, but is not infrequently com- 
bined with other displacements. It may be produced by congenital shortening of one 
of the broad ligaments, by adhesions, or by the pressure of tumors. 

The greater degrees of version may produce very grave lesions. The urethra and 
rectum may be compressed. Cystitis, perforation of the bladder, dilatation of the 
ureters and hydronephrosis, and fatal obstruction of the bowels may follow. If preg- 
nancy exist abortion may take place, or the inverted uterus may be forced through the 
peritoneum and posterior wall of the vagina and project through the vulva. In. the 
non-pregnant uterus pressure on the veins and consequent chronic inflammation of the 
organ may follow. 

Prolapsus Uteri consists of a descent of the uterus into the vagina. The uterus 
may be only slightly lowered or it may project at the vulva. In complete prolapse we 
find a tumor projecting through the vulva, partly covered by the distended vagina, and 
presenting the opening of the os externum near its centre. The bladder and rectum 
may be drawn down with the vagina or may remain in place. The exposed cervix and 
vagina usually become inflamed and sometimes ulcerated, or the mucous membrane may 
become thickened. The lesion is frequently complicated by hypertroph}^ of the cervix. 

Gradual prolapse, which is most frequent, may be due to an increased weight of 
the uterus, as in pregnancy, inflammatory enlargement, the presence of tumors, etc. ; 
or to some abnormal condition of the uterine supports. It is frequently due to vaginal 
cystocele or rectocele. Sudden prolapse is most apt to occur in an enlarged uterus or 
one unduly heavy by reason of tumors connected with it. It is most common in sub- 
involution after parturition. 

Elevation of the uterus is produced by mechanical causes crowding or dragging 
it upward, as adhesions, tumors, etc. The vagina is drawn up and lengthened, and the 
vaginal portion of the cervix may be obliterated. 

Inversion of the uterus consists of an invagination of the fundus. The fundus may 
be invaginated in the body, the fundus and body in the cervix, or the entire organ in 



THE REPEODUCTIVE OEGAXS OF THE FEMALE. 609 

the vagina. It. usually occurs when the uterine walls are relaxed, and may be due to 
traction on the placenta during parturition. It may take place spontaneously after 
parturition. It may be produced by intra-uterine tumors. The mucous membrane of 
the inverted organ is frequently inflamed, particularly when the inversion is complete. 
The epithelium may become squamous and lamellated in type. 

Hernia of the uterus are rare. Ventral liernm may occur during the latter months 
of pregnancy, the peritoneum, aponeuroses, and skin being forced outward to form a 
sac in which the uterus lies. Crural Jiernm are produced by the drawing down of the 
uterus and ovaries into the sac of an intestinal hernia. Inguinal hernia may be pro- 
duced in the same way or be congenital. Isckiatic hernia has been seen. Pregnancy 
may occur in the uterus while it is within a crural or inguinal hernia. 



RUPTURE AND PERFORATION. 

Rupture of the unimpregnatecl uterus is rare. It may, however, 
occur when the uterine cavity is distended with blood or serum, or in 
connection with large myomata of the uterine walls. 

In the gravid uterus ruptures have been seen in nearly every month 
of pregnancy, but most frequently toward the end. The rupture may be 
due to a thinning of the uterine wall by tumors, or by violent contusions, 
or as the result of cicatricial contraction of the os. 

It most frequently takes place in parturition. Malpositions of the 
foetus, narrowing of the pelvis, protracted labor, thinning of the uterine 
wall from tumors, forcible use of the forceps and other instruments, are 
the ordinary causes. The ru]3ture may be in the body of the uterus or 
the cervix, or both ; it may be large or small ; it may extend completely 
or only partly through the uterine wall. The consequences of partial 
rupture are h£emorrhage, gangrenous inflammation of the edges of the 
rupture, peritonitis, and usually death. In rare cases the rupture cica- 
trizes and the patient recovers. Complete rupture usually leads to death 
in a short time. The foetus may escape partly or completely into the 
abdominal cavity. If the patient survive the immediate shock, fatal 
peritonitis usually soon ensues. In rare cases the foetus is shut in by 
adhesions and the patient survives. 

Perforations of the uterus may be produced by carcinoma, by ab- 
scesses in its neighborhood, and by ovarian cysts. 



HYPERiEMI A- UTERINE AND PERI-UTERINE HAEMORRHAGE. 

Hyperaemia. — Aside from the active menstrual hyj)er8emia, the uterus 
may be hypersemic in acute and chronic inflammation, as a result of dis- 
placement of the organ, and in certain forms of heart disease. The organ 
is usually enlarged, the mucous membrane swollen, and the veins are more 
or less evidently dilated. (Edema may be associated Avith hyper?emia. 

Haemorrhage, — Effusion of blood into the cavity of the uterus occurs 

normally at the menstrual periods. For the abnormalities to which this 

function is subject we refer to works on gynaecology. Effusions of blood 

at other than the menstrual periods may be associated with mechanical 

39 



610 THE REPRODUCTIVE ORGANS OF THE FEMALE. 

hyperaemia, hsemorrlioids, acute hypersemia, intra-uterine polypi and 
other tumors, acute and chronic inflammation, typhus fcA^er, scurvy, etc., 
ulcerating carcinoma, abortions, and miscarriage. 

A peculiar form of haemorrhage results in the 80- eddied polypoid hcema- 
toma, OT fibrinous polyj). It occurs after parturition and after abortions. 
The portion of the uterine wall where the placenta was attached, with or 
without a portion of retained placenta, forms the point of attachment of 
the pedicle of the thrombus. A bloody mass is firmly attached by a 
pedicle to the uterine wall ; the uterus enlarges with its formation, the 
cervix is dilated, and the thrombus may project into and fill the vagina. 
The formation of such a thrombus is accompanied by repeated haemor- 
rhages. 

Haemorrhage in the substance of the uterus occurs in arterio- sclerosis. 
The mucous membrane and uterine wall or the cervix are infiltrated with 
blood, and there may be blood in the uterine cavity. 

Peri-uterine or Retro-uterine Hsematocele consists in an accumulation of 
blood around the uterus or in Douglas' cul-de-sac. The haemorrhagic 
mass may become encapsulated with fibrous tissue, or may soften or 
suppurate and perforate into rectum or vagina, or may be absorbed. 
A form of extraperitoneal haematocele is described in which the blood 
lies between the folds of the broad ligament. The extravasation may 
proceed from haemorrhage of any of the abdominal viscera or rupture of 
aneurisms ; from vascular new-formed false membranes ; from rupture of 
the varicose veins of the broad ligaments ; from rupture of haemorrhagic 
cysts of the ovaries ; from the Fallopian tubes in tubal pregnancy or in 
haematometra ; or from general causes, such as scurvy, purpura, etc. In 
some cases the extravasation begins at a menstrual period, and increases 
at the succeeding periods. 

Ante-uterine Hsematocele is of occasional occurrence, either in connec- 
tion with the retro-uterine form or when the posterior cul-de-sac is ob- 
literated. 

ATROPHY, DEGENERATION, ETC, 

Atrophy of the uterus occurs as. a physiological process in old age. 
It may be associated with severe general or infectious diseases or follow 
removal of the ovaries. It may follow pregnancy apparently as an ex- 
cessive involution process. 

Fatty Degeneration. — This may occur in connection with inflammatory 
changes, in acute infectious diseases, and in i^hosphorus poisoning. 

Amyloid Degeneration in the uterus is of rare occurrence. It may 
affect the muscle fibres or the walls of the blood-vessels. 

Phagedenic or Corroding Ulcer. — This rare and little understood form 
of ulceration usually occurs in old age. It begins in the cervix and 
gradually extends until it may destroy the greater part of the uterus or 
even invade the bladder and rectum. The ulcer is of irregular form ; its 
base is rough and blackish, its walls are indurated. It should not be 
confounded with carcinomatous ulcer, which it considerably resembles. 



THE EEPEODUCTIYE ORGANS OF THE FEMALE. 611 

INFLAMMATION. (Metritis and Endometritis.) 

I. Inflammation of the Unimpeegnated Uterus. 

Acute Catarrhal Endometritis. — In this disease, which in its lighter 
grades may leave but little alteration after death, the mucous membrane 
is swollen, hypersemic, and sometimes the seat of jjunctate haemorrhages. 
The epithelium may be degenerated and may desquamate, and the mucosa 
contain an undue quantity of small spheroidal cells. The surface is more 
or less thickly covered with muco- purulent exudate. In severe cases 
shreds of mucous membrane may be exfoliated. The lesion is usually 
most marked in the mucous membrane of the body, but may involve the 
cervix at the same time, or the cervix alone. The body of the uterus 
may be swollen and hypersemic. 

In Endometritis exfoliativa (membranous dysmenorrhoea) there may be 
an exi)ulsion, with more or less blood, of membranous masses consisting 
of fibrin mingled with blood and pus cells, or consisting of exfoliated 
superficial layers of epithelium. This exfoliated epithelium is frequently 
much flattened so as considerably to resemble the vaginal epithelium. 
^^Tien the shreds are large the openings of the uterine glands may be seen 
as perforations. ^ 

Acute catarrhal inflammation of the uterus may be due to injury, ex- 
posure during menstruation, gonorrhceal infection, local infection with 
other bacteria, ^ or it may accompany the general acute infectious diseases. 

Chronic Endometritis. — This may be a continuation of an acute inflam- 
mation or begin as a chronic process. In some of the lesser degrees of 
inflammation but slight changes are found after death. The mucous 
membrane, on the other hand, may be swollen, hyperaemic, and covered 
with muco-purulent exudation. In other cases there is more or less well- 
marked thickening of the mucous membrane, which may present a smooth 
or a rough papillary surface or polyi)oid outgrowths. 

The thickened mucous membrane may show on microscopical examina- 
tion considerable hyperplasia of the uterine glands. These may be fairly 
normal and regular in type ; or the epithelial cells may be much increased 
and irregularly massed within the tubules (Fig. 354) ; the hyperplastic 
glands are often contorted, forming irregular spirals (Fig. 355). The 
interglandular stroma of the mucosa may be little changed or much 
thickened ; it may be dense or very loose in texture and formed largely 
of small fusiform and spheroidal cells. It is often extremely vascular 
and may be tlie seat of interstitial haemorrhage. If there be considerable 
growth of new gland structure the condition is called '^glandular hyper- 
plasia " of the mucous membrane. It is often difficult in the microscopical 
examinations of small portions removed from the uterine mucous mem- 

^See DeWitt, Am. Jour, of Obstetrics, vol. xlii., 1900, bibliography. 

-For an account with bibliography of the bacteria of the vagina see Williams. Am. 
Jour, of Obstetrics, vol. xxxviii.. No. 4, 1898; for bacteria of non-pregnant uterus 
see Miller, Johns Hopkins Hosp. Bulletin, vol. x., p. 29, 1899, bibliography. 



612 



THE EEPEODUCTIYE ORGANS OF THE FEMALE. 



brane by curetting to decide whether the lesion be a simple glandular 
hyperplasia or adenoma. In fact glandular hyperplasia may apparently 
lead to so excessive and unrestrained a growth of glandular structures in 














Jjyi?^ , ' 




Fig. 354.— Chronic Endometritis, Showing Glandular Hyperplasia op the Mucous Membrane. 
The stroma of the mucosa is increased in amount and is dense and flbrous in texture. 

the mucous membrane as to justify the designation adenoma or malignant 
adenomatous hyperplasia. 

Sometimes a thick layer of new-formed, very vascular tissue develops 
over the surface of the mucous membrane, largely covering in the uterine 
glands (Fig. 356). From the decomposition of extra vasated blood in 
the mucous membrane the latter may be mottled with brown or black. 
The glandular elements of the mucosa may be partially or almost entirely 
destroyed. The papillae of the cervix may be hyiDcrtrophied, the mucous 
follicles swollen and their outlets obstructed, leading to the formation of 
the so-called ovula ]S"abothi. The uterine wall becomes flaccid and 







».."^*isf'.' 






Fig. 355.— Chronic Endometritis. 

Showing glandular hyperplasia of the mucous membrane. The stroma of the mucosa is increased in 
amount and is loose in texture. The glands are contorted. 



THE EEPEODUCTIYE ORGANS OE THE FEMALE. 



613 



atrophied, or it may be hyperplastic especially in the cervical portion. 
Ulceration of the mucons membrane, esj)ecially of the cervix, may occur. 
Contraction or obliteration of the cervical canal may occur. 

Fibrous hyperplasia of the cervix with ectasia of the Nabothian 
glands and thickening and erosion or ulceration of the mucous membrane 
is a frequent condition at the climacteric period (Fig. 357). Under these 
conditions both the clinical manifestations and the general appearance of 
the cervix on inspection often suggest the existence of cancer. 

Chronic endometritis may occur at any age, but is most frequent 
after puberty, and is due to a great variety of conditions. It may occur 







Fig. 356.— Chronic Exdometritis with the Formation of a Thick Layer of New-Formed, very 

Vascular Tissue over the Surface of the Mucous Membrane. 

a, Uterine muscle tissue ; 7:), mucous membrane of uterus ; c, new-formed vascular tissue. 

in ill-nourished persons or in those suffering from exhausting diseases. 
It may follow displacements and tumors of the uterus, subinvolution, 
injuries, etc. 

Croupous Endometritis. — This form of inflammation is not very com- 
mon. It occasionally occurs in the puerxDcral uterus, and in acute infec- 
tious diseases. It sometimes involves the vulva, vagina, and Fallopian 
tubes. It may coexist with croupous inflammation of the colon. 

Tuberculous Endometritis. — This is rare and usually occurs as part of 
tuberculous inflammation of the genito -urinary tract. A part or the 
whole of the cavity of the uterus may be lined with a rough, yellowish 
or gray, caseous mass, which may deeply involve the muscular walls of 
the organ. At the edges of the ulcerating caseous areas there may be 



614 THE REPRODUCTIVE ORGANS OF THE FEMALE. 

miliary tubercles, or these may be scattered through the otherwise in- 
tact mucosa. ' 

Syphilitic Endometritis. — This is usually confined to the cervical por- 
tion, and is characterized by shallow or deep ulcerations and condylomata 



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cP//'-^- 






o 



: i^ ■' ' ^- i 




Fig. 357.— Fibrous and Glandular Hyperplasia op the Cervix Uteri. 

The figure shows one side of the cervix in longitudinal section. The fibrous tissue of the cervix is very 
dense and the walls of the blood-vessels are thickened. There is hyperplasia of the glands of the cervical 
canal with erosion of the surface epithelium. The Nabothian glands are distended with clear, glairy fluid, 
(ovula Nabothi). There is erosion of the epithelium at the os externum, and this with the congestion of the 
small superficial vessels here, gave a rough red appearance to the os, suggestive of a malignant growth. 

of the mucous membrane ; or there may be a diffuse thickening of the 
mucosa. 

Acute Metritis is usually associated with acute catarrhal endometritis. 
The organ is swollen, succulent, congested ; the mucous membrane covered 
with muco-pus ; the peritoneal coat congested. There may be small ex- 
travasations of blood in the wall or cavity of the uterus. The inflamma- 
tion, in rare cases, becomes suppurative, and abscesses are formed in the 

^For bibliography see Gullen, Johns Hopkins Hospital Reports, vol. iv., p. 441, 1895. 



THE KEPRODUCTIYE ORGANS OF THE FEMALE. 615 

uterine wall ; these may perforate into the peritoneal cavity or into the 
rectum. 

Chronic Metritis may follow acute metritis or accompanies acute or 
chronic endometritis, and is dependent upon similar conditions : subin- 
volution, displacements, tumors, active irritants, etc. The uterus is en- 
larged, the wall congested, thickened, and soft, or, owing to the new 
formation of connective tissue, hard and dense. The lesion may be most 
marked in the body or in the cervical j)ortion. 

Perimetritis. — The peritoneal coat of the uterus may be inflamed, with 
the production of membranous adhesions or of pus. The adhesions may 
be small or very extensive, and, owing to their contractions, may cause 
various distortions and displacements of the pelvic organs. The inflam- 
mation is usually an accompaniment of chronic metritis and endometritis. 
In prostitutes such adhesions are of very common occurrence. 

Parametritis. — The connective tissue about the uterus, between that 
organ and the reflexions of the peritoneum, may be the seat of suppura- 
tive inflammation. It most frequently ends in death, but may result in 
the formation of dense connective tissue about the uterus. 

II. Inflammation of the Pregnant Uterus. 

The forms of inflammation which have just been described may also 
occur in the i3 regnant uterus. Catarrhal endometritis may lead to effusion 
of serum, extravasations of blood, and abortions. Metritis may lead to 
softening of the uterine wall, so that rupture takes place during labor. 
Perimetritis and iDarametritis produce adhesions and abscesses about the 
uterus. 

Infectious Inflammation (Puerperal Fever), — For a week or more after 
delivery the inner surface of the still dilated uterus is rough, especially 
at the insertion of the placenta, and covered with dark shreds of blood, 
mucous membrane, and placenta. This condition should not, as is some- 
times the case, be mistaken for inflammation or gangrene. 

As a result of injury to the uterus or vagina during or after delivery, 
and the action of bacteria which may gain access to the tissues, in this 
vulnerable state, the puerperal uterus is liable to become the seat of a 
series of severe and often destructive inflammatory and necrotic changes. 
These maybe confined to the uterus; they may induce serious alterations 
in surrounding parts ; they may lead to an involvement of the peritoneum 
or to septicaemia or pysemia and its accompanying lesions in the most 
distant parts of the body. In some cases a more or less extensive gan- 
grenous inflammation of the mucous membrane and the underlying parts 
may lead to the casting- off of larger and smaller shreds of necrotic tissue 
and the formation of deep and spreading ulcers, which may be accom- 
panied by severe parametritis and fatal peritonitis. In other cases the 
inflammation is croupous, and may affect the vagina leading to necrosis, 
gangrene, ulceration, or peritonitis. 

In connection with either of the above forms of inflammation, or 



616 THE EEPRODUCTIYE ORGANS OF THE FEMALE. 

without them, there may be thrombosis of the uterine sinuses, purulent 
inflammation of the veins, suppuration and abscess in the uterine wall, 
suppurative inflammation of the ovaries and tubes, and, owing to the 
generalization of the infectious material, metastatic abscesses in the lungs, 
spleen, kidneys, etc. Or acute pleurisy, ulcerative endocarditis, ery- 
sipelas, purulent inflammation of the joints, hyperplastic swelling of the 
spleen and lymph-nodes, thrombosis or thrombo- phlebitis of the saphen- 
ous veins, etc. , may follow. In some cases which rapidly pass to a fatal 
termination the local lesions may be but slightly marked, and general al- 
terations characteristic of j)y8emia, such as metastatic abscesses, etc., be 






Fig. 358.— Uterine Phlebitis following Delivery; with Retained Placenta. 
Death nine days after delivery. Micrococci in the walls of the inflamed veins stained violet. 

entirely wanting. Death is in such cases api^arently due to toxaemia or 
septicaemia. 

Bacteria are usually present in the exudate, in the lymph-vessels, 
veins, and inflamed tissue of the uterus (see Fig. 358) ; often in enormous 
quantities in the peritoneal exudation and in the metastatic inflammatory 
foci. Streptococcus pyogenes, the gonococcus, B. aerogenes capsulatus, 
and the colon bacillus are the most frequent excitants of the lesion. ' 

TUMORS. 

Fibromata. — Dense nodular fibromata of the uterus are rare, the so- 
called fibromata being in most cases myomata or fibro-myomata. Fibroma 
papillwre, on the other hand, is a common form of growth from the mu- 

' Consult Wadsicorth, " On Puerperal Infection," Am. Jour, of Obstetrics, vol. xliii., 
1901. 



THE EEPRODUCTIYE OEGAXS OF THE FEMALE. 617 

cous membrane. It consists of a more or less vascular connective-tissue 
stroma covered with epithelium. The surface may be smooth or villous. 
It may contain very numerous giancl follicles, and then a^Dproaches the 
type of adenoma, or even carcinoma. The stroma may be loose and 
succulent, and resemble mucous tissue, forming the so-called mucous 
polypi. In any of these forms the blood-vessels may be abundant and 
dilated, forming telangiectatic or cavernous polypi. The adenomatous 
polypi may become cystic from the dilatation of the gland follicles. 

Polyi)i of the uterus may be multiple or single, small or large. 
Numerous smaller and larger papillary outgrowths from the mucous 
membrane may occur in chron- 
ic endometritis. Single polypi /--n;.. ?!;'■« m iv.-v?:'~-^^::;^^;.^> 
may grow from the mucosa of / 

the body of the uterus or from / . 

the cervix, and hang by a long ; - . 

pedicle down into the vagina. i , . t'' 

The large number of glan- p^ '' 

dular structures in many of A i 

these chronic inflammatory, p 

papillary, and polypoid out- / A>' 

growths (Fig. 359) often jus- '\ _ - 

tifies the name of adenomatous ; 

hyj)erplasia of the mucous \ 'v)\ 

membrane or of adenomatous . : , / -'f:^-j 

papillomata or polyps. ' ; iif 

Syphilitic papillary gro^i:hs 
in the form of pointed condy- ^ 
lomata may form finely papil- l 

*lary, wart-like excrescences of v /. 

variable size, particularly on 
the cervix. 

Myomata. — These tumors, 
whose characteristic structural M]&oM^^C:^^j^':^^-Sr:f}:^':::MiJ&^ 

elements are smooth muscle fig. 359.-uterixe polyp— adenomatous or glan. 
cells Tsee Fio' 162^ are the dular polyp of the uterus— polypoid hyper- 

^^ ^' "^-^' plasia of the Mucous Membrane in Chronic Endo- 

most common of uterine tumors metritis. 
and while frequently of little 

practical importance are sometimes of serious import. They are espe- 
cially common in negroes. They are most frequently composed of both 
muscular and fibrous tissue — fibromyomata — but the relative amount of 
the two kinds of tissue is subject to great variation. They are most apt 
to occur after puberty, and usually in advanced life. They may be 
single or multiple, small or of enormous size ; are usually sharply cir- 
cumscribed, whitish or pink, dense and hard, or sometimes soft, and pre- 
sent on section interlacing bands or irregular masses of glistening tissue. 
Their favorite situation is in connection with the body of the uterus, 
but they may occur in the cervix or in the folds of the broad ligaments. 




618 THE REPRODUCTIVE ORGANS OF THE FEMALE. 

According to their position we may distinguish subserous, submucous, 
and intraparietal forms. 

The subserous myomata, often multiple, grow from the outer muscular 
layers of the uterus in the form of little nodules. As they increase in 
size they may become separated from the uterine wall and remain at- 
tached only by a narrow pedicle or by a little connective tissue ; or may 
even be entirely free. They may work their way between the folds of 
the broad ligament until they are at some distance from their point of 
origin. The tumors may become very large, but remain firmly attached 
to the uterus ; this organ may then be drawn upward, the cervix and 
vagina being elongated and narrowed. The traction may be so great that 
the body of the uterus is entirely separated from the cervix. The blad- 
der may also be drawn uj)ward. 

The submucous myomata grow from the inner muscular layers of the 
uterine wall, most frequently in the fundus. They may project into the 
uterine cavity and remain sessile or become pediculated; the uterus 
dilates with the growth of the tumor, and its walls may be also thickened. 

They are usually single, although there may be at the same time sub- 
serous and intraparietal tumors. They are frequently soft. If they are 
of large size and polypoid in form, they may project through the cervix 
and drag down the fundus of the uterus, producing inversion. The 
mucous membrane covering them may be atrophied or hypersemic, with 
dilated blood-vessels, and may thus give rise to severe and repeated 
haemorrhages. In some cases the pedicle of a tumor is destroyed and it 
is spontaneously expelled. 

The intraparietal myomata grow in the substance of the uterine wall, 
but, if they attain a large size, project beneath the serous or the mucous 
coat. They are found in every part of the uterus, but are most frequent 
in the posterior wall. 

The shaiDC of the uterus is altered in a great variety of ways by the 
presence of these tumors ; its cavity is narrowed, dilated, or misshapen ; 
it undergoes flexion or version. The tumors may sink downward and 
become attached to the posterior Avail of the vagina. 

Myomata may undergo a variety of secondary alterations. The mus- 
cle fibres may undergo fatty degeneration and the tumor diminish in size, 
or may even it is said be entirely destroyed. Calcification may occur, 
converting a part or the whole of the tumor into a stony mass. The in- 
traparietal and submucous myomata may give rise to profuse haemor- 
rhages ; they may suppurate and become gangrenous. 

Sometimes the tumors or circumscribed portions of them are very 
vascular, constituting the telangiectatic or cavernous variety. These 
tumors, which possess some of the characters of erectile tissue, may sud- 
denly change in size from a variation in the amount of blood which they 
contain. Larger and smaller cysts may develop within these tumors — 
fibro-cystlc tumors. These may be multiple and may communicate ; they 
may be filled with a clear or bloody fluid. These cystic myomata may 
reach an immense size and fill the abdominal cavity. The cysts may be 



THE EEPEODUCTIYE OEGAXS OF THE FEMALE. 619 

lined with ciliated epithelium. ' Combinations of myoma and sarcoma 
sometimes occur — myosarcoma. 

Myomata of the cervix are rare. They may grow as polypi beneath 
the mucous coat, or produce enlargement of the anterior or posterior 
lips, or may grow outward into the abdominal cavity. 

Myomata of the uterus, either subserous, intraparietal, or submucous, 
containing glandular structures of the type of those in the uterine mucosa, 












4 / ^ ^ At A' 

Fig. 360.— Adexomatous or glandular Myoma of the Uterus. 

are of occasional occurrence (Fig. 360). These glandular or adenoma- 
tous myomata are sometimes directly connected with the uterine mucous 
membrane, but are often so distant and so entirely separated from it as 
to justify the conjecture that they are derived from some embryonal ab- 
normality associated with the development of the Wolffian body.^ Simi- 
lar tumors have been described in the round ligament. ^ 

Sarcomata may occur as primary tumors in the mucous membrane of 
the uterus, either in the form of a diffuse infiltration or as a circumscribed 
nodular or polypoid mass. They frequently involve the muscular wall, 
are liable to haemorrhage and gangrene, and, particularly in the diffuse 
form, are liable to recur after removal. They may consist largely- of 
spindle or spheroidal cells, or both. It is said that sarcoma of the uterus 
is more liable to occur at an advanced age than at an early period, as is 
the rule with sarcomata of other organs. Giant-celled sarcomata have 
been described. 

Angioma. — Cavernous angiomata of the wall of the uterus have been 
described. Endothelioma is of rare occurrence in the cervix. * 

Adenoma. — Between a simple adenomatous hyperplasia of the mucous 
membrane of the uterus, on the one hand (see Figs. 354 and 355), and 

^ Consult monograph by Breus, " Ueber wabre Epitbel. f iihrende Cystenbildung 
d. Uterus-]\lyomen," Leipzig, 1894. 

■^ Culleih ^ohn^ Hopkins Hospital Reports, vol. vi., p. 183, 1897, bibliography. 

^ Cullen, Bull. Johns Hopkins Hospital Reports, vol. ix., p. 142, 1898, bibliography; 
Siho Blum ei', Am. Jour. Obstetrics, vol. xxxvii., p. 37, 1898. 

^Hurdon, Johns Hopkins Hospital Bulletin, vol. ix., p. 186, 1898, bibliography. 



620 



THE REPRODUCTIVE ORGANS OF THE FEMALE. 



carcinoma on the other, there is no absolntely sharj) morphological dis- 
tinction. But there is a considerable group of growths, to which the 









\C' 




! 


"j 


1, 


V 


- ^ ■* 






' n'^ 




■>n 


■f^Y 


■V 


r \l ^ 


•♦ 






H l^V, 






; '> 



V'l- 






' ^ 

\ 






•^A' ^ 



Fig. 361.- Adenoma of the Uterus. 
Showing papillary outgrowths and commencing infiltration of the submucous tissue. 

name adenoma is properly applied, which lie on the border zone between 
the distinctly benign and the definitely malignant new epithelial -tissue 
growths. 

Many epithelial -cell growths of the uterus, while adenomatous in 
structure, are so distinctly malignant, and are so liable to develop that 



„ gOV'""^!', 



^^ 



Fig. 363.— adenoma of the Uterus. 
Showing a small portion of a glandular and papillary growth. 

structural lawlessness characteristic of carcinoma that it has seemed wise 
to many observers to avoid the name adenoma altogether and class all 



THE EEPRODUCTIYE ORGANS OF THE FEMALE. 



621 



Z ^t^ 



^&- 



the epithelial tumors of the uterus amoug the carciuomata. Others, 
recoguiziug the beuigu character of mauy of the epithelial tumors of the 
uterus, have adopted a sharp distiuctiou be- 
tweeu beuigu aud maliguaut adeuoma. ^ ^ 

It seems to the writer wise to preserve 
here, as elsewhere iu the body, the morpho- 
logical distiuctiou betweeu adeuoma aud 
carciuoma. But iu doiug this it should al- 
ways be borue iu miud that the adeuomata 
of the uterus, as those of the gastro-iutestiual 
caual, may uot ouly be extremely maliguaut 
as adeuomata, but that the more beuigu 
forms are extremely proue to develo}), both 
iu structure aud maliguaucy, iuto carciuo- 
mata. Iu fact, iu mauy cases we cau ex- 
press the peculiarities of structure iu these 
tumors ouly by calliug them adeno-carci- 
noma. 

The adeuomata of the uterus may begiu 
iu a simple hyperplasia of the mucous mem- 

braue, iu which glaudular developmeut is prepouderaut (see above). 
AVheu the tumor character becomes established this uew glaudular 
growth is commouly iu the form of irregular, ofteu dilated follicu- 
lar structures with a well-marked lumeu liued with cvliudrical or cu- 





Xrii^«fe 


~ 


'■%-% 




^"'A 


'^^'^ 


4® -'-^.iS 


Adexoma of the Uterus 



'd 



Flfi. 363. 

Showing a small portion of the epi- 
thelium in Fig. 363 more highly mag- 
nified. Mitotic figures are seen in the 
deeper layers. 





vi'^»^Hj 1 


^^f4f V^^ *^JM^K 


^^^^^^^^i"?^ £ ' ■■■ .^^^^^^Bj. 


m.Wm^M 


m 


L .^Fi^^iBH^^^^^^B*r ^^^H^^^^^^^l 


' 


^^W4«kjy,,,.jr 



Fig. 364.— Adenoma op the Uterus. 

Showing the gross appearance of the interior of the uterus with an adenomatous involvement of the entire 

mucosa. 



622 THE EEPEODUCTIYE ORGANS OF THE FEMALE. 

boidal cells. It may develop in irregular papillary masses (Fig. 361), 
the more or less abundant fibrous stroma being covered with irregular 
layers of epithelium (Figs. 362 and 363). The new growth may project 



Fig. 365.— adenoma of the Uterus. 

Showing- the extension of the new growth into the deeper portions of the cervix. The section shows 
one side of the cervix. The epithelium over the portio vaginalis is intact; in the right i^pper region in the 
figure is seen a ragged erosion of the epithelium lining the cervical canal and the exposure of a portion of 
the tumor growth upon the free surface. 

from the inner surface of the uterus in the form of ragged lobular 
masses (Fig. 364), or it may infiltrate the submucous tissues (Fig. 365). 
Or growth in both directions may occur at once. 

The topographical features and clinical stories of many adenomata 
of the uterus are identical with those of the infiltrating and ulcerating 
carcinomata. 

Carcinoma.' — The carcinomata of the uterus commence most frequently 
in the cervix and portio vaginalis, and the most common form is the 
epithelioma. The growth of epitheliomata of the cervix uteri proceeds 
under three tolerably distinct forms which, however, frequently merge 
into one another. 

1. The flat, ulcerating epithelioma. This form of cancer commences 
as a somewhat elevated, flat induration of the superficial layers of the 
cervix, sometimes circumscribed, sometimes diffuse. This induration is 
due to the growth of plugs and irregular masses of epithelial cells into 
the underlying tissue (Fig. 366). Ulceration usually commences early 
1 Consult for details Cullen, "Carcinoma of the Uterus," 1900. 



THE EEPKODUCTIYE ORGANS OF THE FEMALE. 



623 



and may proceed slowly or rapidly. The edges of the ulcer are irregular, 
indurated, and somewhat elevated. The ulceration of the new-formed 
cancerous tissue at the edges is usually progressive, so that the vaginal 
portion of the cervix, the cervical canal, the vagina, and even the blad- 
der and rectum may be involved. More or less extensive haemorrhages 
and necrosis of the base of the ulcer are liable to occur. The entire cer- 
vix may be destroyed. 

2. In another class of cases the carcinomatous growth develops under 
the form of papillary or fungous excrescences, which may form larger or 
smaller masses composed of epitheliomatous tissue. Hand-in-hand with 
this projecting growth there may occur an epithelial infiltration of the 
underlying tissue of the cervix. These growths are often quite vascular 









rT' - - 










''J^n^ 










Fig. 866.— Carcinoma (Epithelioma) of the Uterus. 
Showing ramifying epithelial cell masses. 



and may give rise to severe haemorrhages. They may ulcerate and thus 
produce great destruction of tissue. 

3. In still another class of cases there is a more or less deep infiltra- 
tion of the submucous tissue, either diffuse or in circumscribed nodules, 
with epithelial cell masses. We find at first, in the vaginal portion of 
the cervix, in the submucous connective tissue, either nodules or a gen- 



824 



THE REPRODUCTIVE ORGANS OF THE FEMALE. 



eral infiltration of a whitish new growth. The cervix then appears large 
and hard. Very soon the mncons membrane over the new growth de- 
generates and falls off ; the superficial layers of the new growth undergo 
the same changes. After this the formation of the new growth and its 
ulceration go on simultaneously, i3roducing first an infiltration and then 
destruction of the cervix, and often of a part of the body of the uterus. 
The growth frequently extends to the vagina, the bladder, and the rectum 
with the same destructive character, so that we often find the cervix and 
upper part of the vagina destroyed, and in their place a large cavity with 

ragged, gangrenous, cancerous walls 
(Fig. 3B7). Less frequently the 
pelvic bones are invaded in the 
same way. Not infrequently the 
ureters are surrounded and com- 
pressed by the new growth, so that 
they become dilated. The dilata- 
tion may extend to the pelves and 
calyces of the kidneys. The new 
growth may begin in the cervix 
and extend uniformly over the in- 
ternal surface of the cervix and 
of the body of the uterus. The 
entire uterus is converted into a 
large sac, of which the walls are 
infiltrated with the new growth, 
while the internal surface is ulcer- 
ating and gangrenous. In some 
cases there is a considerable for- 
mation of new, dense connective 
tissue, so that the growth has a 
scirrhous form. 

In rare cases the growth begins 
in the upper part of the cervix or 
in the body of the uterus, while the 
lower part of the cervix is not in- 
volved. In all of these cases the 
epithelial cells of the new growth follow more or less closely the type of 
the epithelial cells of the part from which they spring. But it has been 
observed that carcinomata developing from the mucous membrane of an 
inverted uterus may be of the squamous- celled type. 

In still another class of cases, in which the new growth may be in the 
form of nodules, or diffuse infiltrations, or polypoid masses, or may i)re- 
sent more or less extensive alterations, the cells are irregular, polyhedral 
in shape, the tumor belonging to the class of glandular or medullary 
carcinomata (Fig. 368). These also usually commence in the cervix, 
and, according to the views of many writers, probably in the mucous 
glands. 




Fig. 



367.— Carcinoma of the Cervix Uteri. 
The infiltrating and ulcerating type. 



THE EEPEODUCTIYE OEGAXS OF THE FEMALE. 



625 



In rare cases the entire wall of the uterns is infiltrated with the new 
growth and the organ is ninch enlarged. Gelatinous earcinoma sometimes 
occurs, but is rare. 

AATiile we may for convenience recognize the above types of carcinoma 
of the uterus, it should be borne in mind, as above stated, that thev are 




Fig. 368.— Carcixoma of the Uterus. 
Medullary type. 

often not distinct, and may merge into one another or exist simultane= 
ously. Exudative inflammation is of frequent occurrence in these as in 
other tumors of the uterus. 

As a result of the ulceration of these various forms of carcinoma recto- 
vaginal fistula may be formed ; the lumbar lymph-nodes may be involved, 



J r 









-'^ % 



4^ 









<i^ 



^-c -^-'^- 



FiG. 369.— Fragment of Decidua in Curettings from the Uterfs. 



and metastases in distant organs are occasionally though not often 
formed. Frequent and profuse haemorrhages, gangrenous destruction of 
40 



626 THE REPRODUCTIVE ORGANS OF THE FEMALE. 

tissue, the absorption of deleterious materials, etc. , are apt to lead to the 
development of a more or less profound anaemia and cachexia. 

Deciduoma Malignum. — Under various names several curious tumors 
of the uterus have been described which resemble each other, but which 
differ in structures from any of those in the usual lists. They are, how- 
ever, most closely allied to the sarcomata. They all occur in the uterus 
after pregnancy, and all appear to be derived from remains of the decidua 



\ 






•^ ^ %, ^ 



W% 












''^^ "^^^ "^'-^N "^ .^^€?Vis 



t 'S^^'t! 



r 



# % \ «** 

Fig. 370.— Deciduoma Malignum— Syncytioma. 

or its associated structures (Fig. 369). They frequently give rise to 
haemorrhages and are apt to form metastases, especially in the vagina 
and lungs. 

The structure of these tumors varies considerably. The most typical 
forms consist of irregular clusters or trabeculse of large irregular-shaped 
cells with prominent nuclei or of masses of protoplasm, as well as of 
smaller cells. These cells and cell masses often enclose blood spaces (Fig. 
370). There is relatively little stroma — syncytioma. 

On the other hand, some of the tumors in which the connective-tissue 
elements more largely share are appropriately called Sarcoma deciduo- 
cellidare. 

^yiiether these tumors are derived from the foetal or from the ma- 
ternal tissues is not in all cases clear ; perhaps only one or both may in 
the different cases be concerned iii the growth. ^ 

PARASITES AND CYSTS. 

Echinococcus has been found in the body and neck of the uterus, and 
may rupture into the peritoneal cavity or into the vagina. 

^ For a careful description and consideration of these tumors consult the article by 
Williams in the Johns Hopkins Hospital Reports, vol. iv.. p. 461, 1895; also, for later 
bibliography, Aschoff, "Ergebnisse d. allg. Path.," Lubarsch and Ostertag, Jahrg. v., 
1898, p. 106. 



THE REPRODUCTIVE ORGANS OF THE FEMALE. 627 

Cysts. — Aside from the cysts which develop in tumors of the uterus, 
the mucous follicles in the cervix uteri are frequently so dilated as to 
form cysts filled with a gelatinous material and more or less epithelium. 
These cysts may be large or small, and are frequently called ovula Ncibothi 
( Fig. 357). Sometimes there is an inflammatory growth of new connective 
tissue about these cysts. In other cases the cysts may project from the 
mucous membrane in the form of polypi. Similar changes are infrequent- 
ly found in the body of the uterus from the dilatation of occluded uterine 
glands. Dermoid cysts are rarely found in the walls of the uterus. 

Lesions of the Placenta.' 

Aside from the variations from the normal in size, shape, and posi- 
tion, for a description of which we refer to the works on obstetrics, we 
may briefly mention here some of the more important structural changes 
which the placenta may undergo. 

DEGENERATION. 

Fatty and amyloid degeneration and calcification of the placental tissue 
are of not infrequent occurrence. 

H-ffiMORRHAGE. 

This may occur either on the maternal surface in the decidua, or 
between the foetal surface and the membranes, or in the substance of the 
placenta. The latter form of haemorrhage constitutes the true placental 
aimplexy. This may occur as the result of rupture of a placental sinus. 
The placental tissue is crowded apart, and a blood clot, often infiltrating 
the parenchyma, is formed. This may lead to abortion, or the blood 
may undergo disintegration and absorption and its place be occupied by 
a cicatrix. ■ The placental tissue in its vicinity may undergo fatty degen- 
eration. Under other conditions, without evidence of rupture of the 
vessels, the placental tissue may become infiltrated with blood in the 
form of an infarction. In this, degenerative changes similar to the above 
may occur, leading to fibrous induration of the placenta. 

The so-called ^infarctions" of the placenta vary in size, appearance, 
structure, and origin. They are most frequently due, according to 
Williams, to an endarteritis of the vessels of the chorionic villi. They 
appear to be of little significance when of moderate size. ^ 

INFLAMMATION. (Placentitis.) 

Suppurative Inflammation of the placenta, Avith the formation of ab- 
scesses, is of rare occurrence as the result of injury. 

^ For a study of the placenta, normal and pathological, see Eden, Journal of Path. 
andBact., vol. hi., p. 449, 1896, and vol. iv., p. 265, 1897, bibliography. 

'^ For a study of placental infarcts see Williams, " Welch Anniversary Contr. to 
the Science of Medicine," 1900, p. 431, bibliography. 



628 THE REPEODUCTIYE ORGANS OF THE FEMALE. 

Chronic Indurative Inflammation of the placenta may result in the for- 
mation of circumscribed masses of cellular and loose, or dense and cica- 
tricial, connective tissue, or in a diffuse formation of connective tissue, 
which may interfere with the nutrition of the foetus and cause abortion. 
The new-formed connective tissue may undergo fatty degeneration or 
calcification. 

In another class of cases the new connective tissue is formed mainly 
in the walls of the vessels, particularly the arteries. This may occur in 
circumscribed portions of the vessels, leading to nodular growths around 
the arteries, or it may occur extensively along the various ramifications 
of the vessels, converting them into thick fibrous cords. The change is 
primarily in the adventitia, but all the coats of the vessel may become 
involved, leading to more or less complete obliteration of the lumen. 

Various proliferative and indurative changes in the placenta may 
occur as the result of syphilitic inflammation. 

Tuberculous inflammation of the placenta may occur in connection with 
other tuberculous processes in the mother. 

TUMORS. 

Fragments of placenta remaining in the uterus after delivery may 
serve as a nidus for a blood thrombus, or they may undergo prolifera- 
tion, thus forming tumors, deciduomata. 

An hypertrophy of the villi of the chorion may give rise to the fibrous 
structures known as fibrous moles. When to the fibrous change mucous 
degeneration is added the so-called hydatid moles are formed.' 

Cysts of the placenta are of occasional occurrence ; their origin is in 
most cases obscure.^ 

The Ovaries. 

Malformations. 

One or both ovaries may be absent, the other organs of generation being also absent 
or undeveloped ; or they may be only partially developed. Absence or arrest of devel- 
opment of one ovary occasionally occurs in otherwise well-formed individuals, and is 
sometimes accompanied by a low position of the kidney on the same side. The ovaries 
may pass into the inguinal canal or into the labia majora, and remain fixed there 
through life. Less frequently they are found in the crural canal or the foramen ovale. 

Changes in Size and Position. 

The ovaries may become larger than normal by chronic inflammation, by the forma- 
tion of cysts and tumors. They may become atrophied in old age, the Graafian follicles 
disappearing and the organ shrivelling into a small, irregular, fibrous body. Atrophy 
may be produced hy ascites, by chronic inflammation, or from unknown causes. As 
the result of the maturing and rupture of the Graafian follicles, with and without preg- 
nancy, the surface of the ovary, which before puberty is smooth, may become rough- 
ened by irregular cicatricial depressions. 

^ Consult MarcJiand, Zeits. f. Geburtsh. u. Gynak., Bd. xxxii., p. 405; also Fraenkel, 
Arch. f. Gynak., Bd. xlix. 

^ See Ahlfeldt, Arch, fiir Gynakologie, Bd. ii., p. 397. Fenomenodes, ibid., Bd. xv. 
p. 343. Hofmeier, "Die menschliche Placenta," 1890. 



THE EEPRODUCTIYE OEGAXS OF THE FEMALE. 629 

In adult life the ovaries may pass as bernige into the inguinal or crural canal, the 
fwamen ovale, or the umbilicus. Their position in the abdomen may be changed by 
the pressure of tumors, the traction of false membranes, etc. This may occur in en- 
larged ovaries or in those of normal size, and by the compression of the veins may lead 
to congestion and chronic inflammation of the organs. 

HYPERiEMIA AND H-SlMOilRHAGE. 

Aside from the normal liypersemia of the ovaries during menstrua- 
tion, the vessels may be congested in inflammation, in displacements with 
interference with the venous circulation, in certain diseases of the heart, 
etc. , and may then be followed by chronic inflammation. 

The menstrual periods are accompanied by the effusion of blood into 
a Graafian follicle. Xormally the amount of blood is small, becomes 
solid, is decolorized, and then gradually absorbed. Sometimes the effu- 
sion of blood is much greater ; the follicle filled with blood is as large as 
a i)igeon's egg. The blood may remain in the follicle and be absorbed, 
and replaced by a serous fluid, or through rupture it may escape into the 
peritoneal cavity. Death may ensue from the haemorrhage, or the blood 
may collect in Douglas' cul-de-sac and become encapsulated. Haemor- 
rhages also occur in follicles which have become cystic. Interstitial 
haemorrhage in the ovary sometimes occurs without known cause. 

INFLAMMATION. (Oophoritis.) 

Acute Exudative Inflammation of the ovaries occurs most frequently in 
the puerperal condition, either as part of a general peritonitis or as a 
primary affection. 

With puerperal peritonitis both ovaries are usually inflamed ; they 
are swollen, congested, soft, infiltrated with serum or pus, or gangren- 
ous. The lesion may involve principally the capsule, the stroma, or the 
follicles. Inflammation of the capsule results in adhesions and collec- 
tions of pus, shut in by false membranes ; of the stroma, in abscesses and 
fibrous induration; of the follicles, in their dilatation with purulent 
serum. 

If the inflammation of the ovary be the primary lesion it is usually 
confined to one organ. The stroma of the ovary is infiltrated with serum 
and pus, and may contain abscesses of large size. In other cases the 
ovary itself is but little changed, but is surrounded by a mass of fibrin- 
ous and purulent exudation. Such independent forms of ovarian inflam- 
mation may terminate in recovery ; or the abscesses may perforate into 
the rectum and vagina ; or the ovary is left indurated and bound down 
hj adhesions ; or the patient may die. 

Acute exudative inflammation of the ovaries unconnected with the 
puerperal condition is not common, but it may occur in connection with 
acute or chronic peritonitis or jDerimetritis, with various infectious dis- 
eases, i^yaemia, etc. It is usually confined to one ovary. 

Chronic Interstitial Oophoritis is not infrequently^ preceded by an acute 
inflammation, or it may gradually develop as an independent condition. 



630 



THE REPRODUCTIVE ORGANS OF THE FEMALE. 



often determined by some mecliamcal interference with the blood cur- 
rent. The organ may be increased in size, owing to the formation of 
loose cellular or of dense, firm, new connective tissue. Under these 






^ £0''^r^ ^ 



Fig. 371.— Chronic Oophoritis with Dilated Blood-Yessels and Cysts. 

a, Dense connective-tissue stroma ; Z), dilated veins ; c, cysts ; c?, cyst with granular contents ; e, corti- 
cal zone of immature Graafian follicles. 

conditions the blood-vessels, especially the veins, may be widely dilated, 
and cysts in varying number and size may be present (Fig. 371). Some- 



^. y 










V 




Fig. 372.— Chronic Oophoritis with Atrophy. 

From a case of valvular disease of the heart with chronic metritis and endometritis, a. Thickened and dense 
interstitial tissue ; h, old corpora lutea ; c, arteries with greatly thickened walls ; c?, dilated veins. 



times the new-formed dense connective tissue may be largely limited to 
the surface of the organ, so that the albuginea may become dense and. 



THE REPROBUCTIYE ORGAiMS OF THE FEMALE. 631 

thick. Under these conditions the surface of the ovary may be smooth 
or rough. 

On the other hand, the organ may be smaller than normal as the re- 
sult of the formation of dense new interstitial connective tissue, and its 
surface greatly roughened and distorted (Fig. 372). Sometimes the 
formation of new dense tissue may be largely confined to the walls of the 
arteries, which become prominent and tortuous. Obliterating endarte- 
ritis is not infrequent. The atrophied ovary may be largely made \i]) of 
thick-walled arteries and of fibrous masses which are the result of incom- 
plete resolution of the corpora lutea. 

Occasionally a more or less extensive hyperplasia of cells in the corpus 
luteum leads to the dcA^elopment of larger or smaller new-formed, convo- 
luted, nodular masses in the ovary, which are sometimes regarded as 
tumors. Sarcomata of the ovary apiDcar to originate in such an hyper- 
IDlasia (see Fig. 374). 

Tuberculous Inflammation of the ovaries is rare, and may accompany 
tuberculous inflammation of other organs, particularly the peritoneum 
and Fallopian tubes. It usually results in the production of dense case- 
ous nodules of considerable size. 

Syphilitic Inflammation in the form of gummata is uncommon. 

TUMORS. 

Fibroma is not common nor usually of great importance. Such tumors 
may be small or large. They are usually dense in texture, and seem often 




Fig. 373.— Papilloma of the Ovary. 

to originate in the tissue formed in the closure of the ruptured Graafian 
follicle. They may contain cysts or be accompanied by cysts of the sur- 
rounding stroma. Papillary fibromata of the surface of the ovary are 
sometimes seen (Fig. 373), and the growth may be transplanted from this 
situation to the general peritoneal surfaces (Fig. 304, page 525). 



632 



THE KEPEODUCTIVE ORGANS OF THE FEMALE. 



Chondroma of the ovaries is described, but is rare ; cartilage not infre- 
quently occurs, however, in dermoid cysts. 

Leiomyoma containing more or less fibrous tissue is of occasional oc- 
currence. 

Sarcoma of the ovaries is not common. It is usually primary, and 
may apparently develop from the ne\Y- formed cells of the corpus luteum 









Fig. 374.— Commencement of Sarcomatous Growth in the Ovary. 
From hyperplastic cells of corpus luteum. 

(Fig. 374), but may be metastatic. It is usually of the spindle-celled 
variety, but may contain areas of spheroidal -celled tissue or more or less 
fibrous tissue. The tumors may be hard or soft, and are apt to involve 
both ovaries. Endotheliomata may be found in the ovaries (Fig. 375). 

Carcinoma, usually of the medullary variety, may occur as a j^rimary 
tumor of the ovary. It may be due to a continuous extension from 
neighboring organs, or more rarely it is of metastatic origin. Although 
the medullary carcinomata are the most common, scirrhous, melanotic, 
and gelatinous forms sometimes occur. Some types of carcinoma stand 
in very close relation with certain of the cystic adenomata (see below). 

Adenoma (Cystic Adenoma ; Compound Ovarian Cyst). — These growths, 
which may occur in one or both ovaries, form one of the most common 
and im]3ortant classes of ovarian tumors. They probably originate in 
the gland epithelium of the ovary either before or after the formation of 
the Graafian follicles. Some of their most noteworthy and im^^ortant 
features depend upon their tendency to the formation of cysts. It should 



THE REPRODUCTIVE ORGANS OF THE FEMALE. 



633 



be remembered, however, that the primary lesion is a true new formation 
of glandular tissue, and not, as in the case of most cysts, a transforma- 
tion, bj" retention or otherwise, of pre-existing structures. 

The growth primarily consists of a fibrous stroma in which are tubu- 
lar follicles lined with cylindrical epithelium — glandidar type. Or, in 
some cases, it consists of papillary outgrowths from a fibrous stroma, 
which are covered with cylindrical epithelium — papillary type. 

Glandidar Cystadenoma. — There is, as above stated, a marked ten- 
dency, in this form of adenoma, to dilatation of the follicles by a semi- 
fluid material, and the formation of cysts. There may be a number of 
follicles equally dilated, so as to form a number of cysts of moderate size 
(Fig. 376) ; or a few follicles are enormously dilated to form a large 
midtUocular cyst with but few compartments. The walls of the cysts may 
fuse together and be absorbed, so as to form one large cyst divided by 
incomi)lete septa — unUocidar cysts. The stroma in which the follicles and 
cysts are embedded may be largely developed or very scanty. 

The walls of the larger cysts are composed of fibrous tissue which is 
dense in the outer layers, more cellular in the inner, upon which the 
epithelium is placed. They may be thin and membranous, or there is 
upon their internal surfaces an iutracystic growth composed of a fibrous 




Fig. 375.— Endothelioma of the Ovary. 



stroma and tubular follicles. These secondary follicles may also be filled 
with fluid and form larger and smaller cysts. The intracystic growths 
may be so large as to fill up the original cysts. Sometimes the intracystic 
growth presents very little dilatation of its follicles, so that the entire 
tumor has more the character of a solid growth than of a cyst. 



634 



THE EErEODUCTIYE OKGANS OF THE FEMALE. 



The cyliudrical epitlielium liuiug the cysts usually forms a single layer 
(Fig. 377), but several layers often irregular in thickness may form, and 




^»fO 




/I 



'0 ^-.^^ ^-^^^r^^iP- -^^ 




Fig. 376.— Cystadenoma of the Ovary— (Multilocular Ovarian Cyst— Adeno-Cystoma). 
This photograpbic reproduction is about four-flfths natural size. 

owing to the accumulation of fluid the cells may become flattened and 
atrophied, or they may be fatty or desquamated. The contents of the 







?'-'^v 




f<mm 



Fig. 377.— Cystadenoma op the Ovary— Glandular Type. 



cysts differ considerably in different cases, and even in different cysts in 
the same case. They may be tough and ropy, or gelatinous or serous ; 
transparent and colorless, or yellow or reddish, or reddish-brown; or 
they may be turbid and colorless, or variously colored — red, brown, or 
cliocolate. 



THE EEPEODUCTITE OEGANS OF THE FEMALE. 



635 



Chemically the cyst contents, when thick and ropy, include mucin or 
paralbumin, and perhaps other less well-known comj^ounds belonging to 
the same class. It is probable that the contents of these cysts are, so far 
as the mucin and paralbumin are concerned, produced by a metamor- 
phosis of the protoplasm of the lining cells, similar to that by which the 
mucin is produced in the mucous glands and in mucous membranes. 
The cylindrical cells often present the form of the so-called '^beaker 
cells, ^^ and in some cases the mucous contents of the cysts are seen to be 
continuous with the similar contents of the beaker cells. It is probable 
that much of the fluid contents of the cysts comes from simple transu- 
dation. 

Microscopically the contents of these cysts present also considerable 
variation. We may find almost no structural elements, or there may be 




Fig. 378.— Ctstadexoma of the Otart— Papillary Type. 



red blood cells in variable quantity, and leucocytes in various stages 
of granular or fatty degeneration or of disintegration. There may be 
cylindrical, or flattened, or polyhedral cells, either well preserved, swol- 
len, or in a state of fatty degeneration, or fragments of these cells. 
It is these various forms of cells, often more or less swollen and in a con- 
dition of more or less well-marked granular and fatty degeneration, which 
have been considered characteristic of the ovarian cysts and are some- 
times called BrysdaJe^s corpuscles. While, however, they are of frequent 
occurrence under these conditions, they are by no means pathognomonic, 
since we find them in the contents of various kinds of cysts and cavities 
where the cells are undergoing degeneration. In addition to the above 
structural elements we may find free fat droplets, cholesterin crystals, 
pigment granules, and more or less granular detritus. The gelatinous 



636 



THE EEPEODUCTIYE ORGANS OF THE FEMALE. 



material filling these cysts is sometimes called colloid, and the cysts are 
frequently called colloid cysts. 

iN'umerous secondary changes are liable to occur in these cysts. The 
cells may peel off, the walls of the cysts atrophy or become calcified. 
Suppurative inflammation, perforation into the peritoneum, bladder, 
vagina, or rectum; haemorrhage, gangrene, etc., may occur. As a re- 
sult of chronic jDroductive processes, the cyst \Yalls may become thick- 
ened and extensive adhesions may form. Carcinoma may develop from 
these tumors. 

PcifpUlary Cystadenoma. — This type of cystadenoma was formerly re- 
garded as but a variety of the form above described — a variety charac- 
terized by papillary outgrowths in cauliflower-like tufts from the walls 
of the cysts, which often in large degree fill the cyst spaces (Fig. 378). 




FIG. 37 



-Multiple Papillary Cysts of the Omentum, Secondary to a Similar Growth in the 

Otary. 



The papillary outgrowths are themselves hecoming softened at their centres, forming accessory cysts. 



There appears, however, to be sufficient evidence, both anatomical and 
clinical, to justify the separation of the papillary from the glandular 
form of cystadenoma. 

The papillary cystadenomata are not, as a rule, as large as the gland- 
ular form. The cysts are fewer and they do not contain colloid material. 
The papillary outgrowths often break through the cyst walls, and may 
be transplanted to the peritoneal or other surfaces in the form of multiple 
cystic or papillary tumors (Fig. 379). The papillae and cyst walls may 
be lined by cylindrical and often by ciliated epithelium. ' 

Follicular Cysts of the Ovary. — The Graafian follicles may be dilated so 
as to form cysts. This may occur in one or both ovaries, and the cysts 
may be small or large, single or multiple. They are usually found after 
middle life, but may occur during youth, childhood, or even in the foetus. 

^ For reference to bibliography of these ovarian cysts see Russell, Johns Hopkins 
Hosp. Bulletin, vol. x., p. 10, 1899. 



THE REPRODUCTIVE ORGANS OF THE FEMALE. 637 

The follicles dilate from the accumulation of fluid within them ; the ovum 
is destroyed, the epithelium flattened. The contents are usually serous 
and colorless, but may be viscid, turbid, purulent, or variously colored, 
red, yellow, or brown. The ovary may be crowded with numerous cysts 
of moderate size, whose adjacent walls may coalesce and atrophy, form- 
ing communications between them. ^ 

A variety of this type of cyst is formed by the dilatation of a corpus 
luteum either with or without the hyperj^lasia of the wall. 

Dermoid Cysts. — These cysts may be uni- or multilocular, are usually 
of moderate size, but sometimes become as large as a man's head or 
larger. Their fibrous walls may be thick or thin, and portions of the 
internal surface may i)resent more or less completely developed cuticular 
structures, such as corium, papillse, epidermis, hairs and hair follicles, 
sebaceous glands, etc. The cavity may contain a thick, whitish, greasy 
material composed of flattened ex)ithelium, fat, or cholesterin crystals. 
Or the cavity or walls may contain masses of irregularly formed hair, 
teeth, bone, cartilage, striated muscle, and nerve fibres and cells. '^ Such 
growths, which are doubtless of embryonal origin, may exist for many 
years without causing inconvenience; but inflammatory changes may 
occur in them, leading to adhesions and perforations into adjacent organs. 
They may form the nidus for the development of carcinoma, or they may 
calcify. 

In addition to the above -described adenoid, dermoid, and simple fol- 
licular cysts, there are a number of composite forms of not infrequent 
occurrence. Thus, in connection with dermoid cysts or separately, there 
may be simple ciliated cysts or those which partake of the characters of 
both adenoid and dermoid cysts. These may be multilocular and be 
lined with flattened, cylindrical, or ciliated epithelium, and may contain 
epidermal cells, cholesterin or mucin, etc. 

Small cysts, sometimes pediculated, sometimes not, of doubtful origin 
and usually of no special significance, are frequently found growing from 
the broad ligament near the ovary. The walls are usually very thin, 
lined with flattened epithelial cells, and the contents serous. 

Teratomata not cystic are of occasional occurrence in the ovary. ^ 

Cysts of the Parovarium, lying between the peritoneal layers of the 
broad liagment, are usually small, but may be as large as a man's head. 
They are usually lined with ciliated epithelium, but sometimes with flat- 
tened non-ciliated cells. The contents may be serous, or may be thick 
and contain mucin and paralbumin. 

' r. KaJilden. Ziegler's Beitr., Bd. xxvii., p. 1, 1900, bibliography. 
"^For a study of the origin of dermoid cysts of the ovary see Amsperger, Virchow's 
Arch., Bd. clvi., p. 1, 1899,'bibliography. 

3 Consult Wilms, Ziegler's Beitr. z. path. Anat., Bd. xix., p. 367, 1896. 



638 



THE REPRODUCTIVE ORGANS OF THE FEMALE. 



The Fallopian Tubes. 

Malformations . 

Absence of both tubes occurs with absence of the uterus. One tube may be absent, 
with arrested development of the corresponding side of the uterus. Both tubes may be 
imperfectly developed ; either of their ends may be closed ; they may be inserted into 
the uterus at an abnormal place ; they may terminate in two or three abdominal ostia. 

Changes in Position and Size. 

The Fallopian tubes may participate in the various malpositions of the uterus and 
ovaries; but they are most frequently displaced by the contraction of adhesions formed 
in perimetritic and periovarial inflammations. 

The lumen of the tube may be partially or completely closed as the result • of in- 
flammation of the mucous membrane ; of peritonitis about the fimbriated extremity ; 




Fig. 380.— Hydrosalpinx— Schematic. 



of tumors or inflammation of the uterus ; or by pressure from without, or by adhesions, 
tumors, etc. It may become stopped by plugs of mucus or pus. 

Dilatation of the tubes may be produced by an accumulation of catarrhal or other 
exudation, when there is partial or complete stenosis at some portion of the tube. The 
dilatation may be moderate, converting the tube into a tortuous, sacculated canal con- 
taining mucous or serous fluid ; or, more rarely, large cysts may form containing several 
pounds of serous fluid — hydrosalpinx^ (Fig. 380). As the fluid collects the epithelium 
may become flattened or fatty or may desquamate. Inflammation may take place in 
the walls of the dilated tube and the contents may be mixed with pus or blood. Rup- 
ture of a dilated tube sometimes occurs ; or severe and even fatal haemorrhage may take 
place into its cavity. Papillary growths are sometimes found springing from the inner 
wall of the cyst. 

HiEMORRHAGE. 

Hgemorrhage into the tube may occur in puerperal women with retro- 
version of the uterus, with abortions; haematometra and tubal preg- 

^ For a study of hydrosalpinx with full bibliography see Cullen, Johns Hopkins 
Hospital Reports, vol. iv., p. 351, 1895. 



THE REPRODUCTIVE ORGANS OF THE FEMALE. 639 

nancy ; in acute infectious diseases. The blood may undergo degenera- 
tive changes and be largely absorbed, or it may escape into the peritoneal 
cavity and cause peritonitis. 

INFLAMMATION. (Salpingitis.) 

Catarrhal Inflammation of the mucous membrane of the Fallopian tubes 
commonly occurs in connection with endometritis, frequently in the puer- 
peral condition. In the acute stage the mucous membrane is hypersemic 
and swollen, and covered with a mucous or muco-puruleut often bloody 
exudate. The inflammation may subside, leaving no lesions, but it more 
frequently becomes chronic, and may then result in peritoneal adhesions, 
thickening of the walls, obliteration of the tubes, dilatation, etc. ; or the 
mucous membrane may undergo hyperj)lasia with papillary outgrowth. 
Such x)apillary masses may partially coalesce, forming on the accumula- 
tion of fluid, cyst-like cavities lined with epithelium. Hyperplasia of 
the muscle wall of the tube may be associated with these conditions. ' 

Suppurative Salpingitis. — Catarrhal inflammation of the mucous mem- 
brane may assume a sui^purative character, sometimes in connection with 
puerperal metritis and peritonitis, and often as a result of gonorrhoeal 
infection. Under these conditions the wall of the tube may be involved 
and pus may exude from the abdominal ends. It is difficult, in many 
cases of suppurative salpingitis associated with peritonitis, to say which 
is the i^rimary lesion. 

If the abdominal end of the tube be closed by adhesions or otherwise 
there may be a considerable collection of pus in the tubes, causing dila- 
tation — ijyosal])inx. Such a collection may rupture into the peritoneal 
cavity, or the pus may escape into a cavity shut in by adhesions, or may 
perforate into the intestine or bladder. Or it may dry and finally become 
calcified. 

Suppurative salpingitis is most commonly incited by the gonococcus 
or the pyogenic bacteria. 

Tuberculous Inflammation. — The lesions are most frequently seen in the 
later stages of the process, when the inucous membrane is partially or 
entirely converted into a thick, caseous, often ulcerating layer. The 
lumen of the tubes may be dilated, and the walls thickened from chronic 
inflammation. This lesion may occur by itself, or may be associated with 
tuberculous inflammation of the lungs, or of the other genitourinary 
organs, or of the peritoneum. It usually commences at the abdominal 
ends of the tubes, and both tubes are apt to be involved. 

Syphilitic Inflammation, manifested by a diffuse fibrous thickening of 
the wall, has been described. 

TUMORS. 

Small fibromata and fibro-myomata sometimes occur in the wall of the 
tubes or in the fimbriae. Small lipomata have been seen between the folds 

'Consult Pdes, Jour. Exp. Med., vol. ii., p. 347, 1897, bibliography. 



()40 T\\\: u\]vno\n'cTi\\] okujans ov tuv: vv.swxa:. 

oi' tho broad ligaiiUMit in clost^ coniuH'tion witli Hk^ (uIh^s. Papillomata 
arc v:\\\\ 

Carcinoma of the tubovs is usually, if not always, socondary to carci- 
noma oi' tho uterus or tho ovaries. 

Cysts, usually oi' small siz(\ sometimes pediculated and with thin 
walls, are ircHiuently sihmi in the piM'itoneal eoviM-iuix oi' the tul)es or in 
the tiud)ria\ They are believiHl to l)e oi' end)ryonal oriiiin. (\>ud>ina- 
tion eysts of the tul>es and o\arit's are oi' oi'easional oeeurrenee — retro- 
ovarian eysts. ' 

Dilatation oi' the tubes, as al>ove described, may convert them into 
cyst -like stnu'tures. 

Extra-Uterine Pregnancy. 

TriiAii PuFA;^'A^'CY. — Tho iniprogiiatod ovum, in sonu' way hindorod frem passing 
into the uterus, may become tixed in the t\ibe, antl there develop. The villi of the 
chorion grow into the mucous membrane of the tube, forming an incomplete plaeenta. 
Kare cases are recorded in which the placenta was situated in the uterus while the 
fa^tus was develinHHi in the t\die. The end>ryo and its mendiranes are developed until 
they reach such a size that the tube surrounding them ruptures. This may oeeur in the 
lirst month or not until much later. In mre cases. Avhen \\\c ^vall of thi> tub(> was ex- 
tensively involved in the formation of tlie placenta, the development has gmie on until 
term. The ovum may remain in the tube after the rupture, or may escape into the 
peritoneal cavit\-. still enveU>ped in its mendu-anes: or the membranes may be ru]Uured 
and left in the tube. The rupture is generally attendxHl with fatal luvmorrhage. In 
some cases death is caused by the rupture of a di1aie*l vein while the tube is still intact. 
Ihcmm-rhage into the sac may occur before its rupture. 

In rare cases death (hH>s not take place and the t\ctus is shut in by adhesions and 
false membranes. The embryo soim dies. There may be a slow absorptitm of the soft 
parts of the ftvtus. the bones are separated and left embeilded in a mass of fibrous tissue, 
fat. cholesterin, and pigment; or the foetus retains its shape antl becomes nnunmitied, 
and may then be encrusted with the salts of lime (lithopedion). 

On the other hand, degeneration and gangrene of the fivtus may take place rapidly, 
with inflammation and suppuration of the siu-rounding tissue. There may be perfora- 
tion and escape of the broken-dcnvn ftrtus through the rectum, vagina, bladder, or ab- 
dominal wall. The patient may die from peritonitis Or exhaustion, (U* may recover 
after the escape of the fivtus. In some cases the ftvtus may escape through a rupture 
of the tube into the space between the folds of the broad ligament. 

In Tuno-AnnoMiNAi: Pkegx.v^-cv the development of the ovum is in the tlmbriatcd 
extremity of the Fallopian tube. Adhesions are formed, so that the fivtus is partly in 
the end of the tube and j^artly in the abdomen. 

iNTKiiSTiTiAi. PuKc; NANCY. — Thc ovuui iu tlu'sc casos is arrcstod and deveh^ped in 
the ]iortion of the tube which passes through the wall of the uterus. 

Aiu^oMTXAT- Pkegnancy. — Thc ovmn. after escaping from the ovary, may not 
enter the Fallc>pian tube, but may beciMue tixed t(^ the periti^ieum. usually near the 
ovary, and develops in that position. 

OvAiuAN Pregnancy. — The existence of this form of pregnancy is doubtful and 
difficidt to prove, but there are some cases in which it seems probable that the ovum 
develops in its Graafian foUiele. The placenta maybe attached to the tube or to the 
abdominal wall. 

In all forms of extra-uterine pregnancy the uterus beci^mcs enlarged and a sort of 
decidua is formed on its internal surface. 

^ See OrtJimann, Yirchow's Arch., Bd. civ., p. 0*20, 1S99, bibliography. 



Tin: JiKi'iiOJXT'j ni. o]if;A\s or -jin. j-kmalj;. 041 

The Mamma. 
Malformations . 

Arrest of development of the rriamma; occurs with arrest of deveJoprnf.nt, of the 
other reproductive organs, and less frer^uently alone. 

One or both mammae may he absent. Absence of iIjc nipple is more comnjon. 

Superniimerary mauima; and nif^ples have be-en observed in a nunjf;er of cas^-s; the 
glands may all secrete milk during lactation. 

Too early development of the mammaj is sometimes found in young children in 
connection with abnormal development of the organs of generation. 

HEMORRHAGE. 

In youri^ women who suffV^r from anif^norrho^ja or dy.srnenorrhr/ia, 
Hmall haemorrhages sometimes occur in the yii'dinni'dt at the time of irjeii- 
struation. The blood may find its way into tlie milk ducts and exude in 
small (J uaii titles at the nipple. 

Contusions of the breast may f>roduce extravasations of hJood in the 
mammary gland or the surrounding^- connective tissue. TIji's ruay become 
absorbed, or may remaiu and be surroundr-d by fibrous tissue or be con- 
verted into cysts. 

INFLAMMATION. rMastitis.) 

During lactation the nipjde is Jiabht to beconje infiamed, and ulcers 
and h.ssures may form. 

There is a form of eczematous inflammation of the nipjjle and areola 
which tends to ulcerate and in which carcinoma may originate. This 
is known as Paget's disease, and is probably due to the i>resence of 
cocci di a. 

Acute Exudative Inflammation ^Mastitis;.— This occurs mo.st frequently 
during lactation; it also occurs durijjg pregnancy, and occasionally in 
women AV'ho are neither pregnajjt nor nursing. 

The process may involve the subcutaneous connective tissue, the 
gland it.sfdf, or the coirnective tissue between the glajjd and the wall of 
the thorax. The inflamed ti.ssues are at first congested, swollen, hard, and 
painful. The inflammation may stox> at this i>oint and resolution may 
take x>lace, but more frequently it is succeeded by sujipuration. If the 
inflammation involves the subcutaneous connective tissue the abscess may 
be suijerficial and may soon open through the skin. If the gland be in- 
volved one lobule after another may become affected TFig. 381;, so that 
successive abscesses are foiTued. If the connective ti.ssue beneath the 
gland be inflamed a deex> abscess of large size may I>e formed, which usu- 
ally jierforates through the skin, but sometimes into the ydeural ca\'ity. 
In both these latter forms of abscess there is ax>t to be necrosis of large 
portions of tissue. Thes^- abscesses may cicatrize, or they may pass into 
a chrojjic condition and remain for a long time as sujiXjurating, fi.stnlous 
41 



642 



THE REPRODUCTIVE ORGANS OF THE EEMALE. 



tracts. Suppurative mastitis is usually due to the preseuce of Strepto- 
coccus and Staphylococcus pyogenes. 

In new-born children there is often a painful swelling of the breasts, 
which usually subsides in a few days, but may go on to suppuration. 



l^Wf^^^^^^^^&^^^'^^^^^^^^^^^^S^^^^^^ 




^"-.^^y '^-^ 







s^^Mft- -^^ ^^M^^^^M 



|p^|pi^Xii;^^lll^iij|^^^ 



Fig. 381,— Suppurative Mastitis in the Non-Functionating Gland. 
a. Milk duct ; h, interstitial tissue ; c, dense collections of pus ; (?, diffuse infiltration of lobule with pus. 

Epidemic parotitis is sometimes complicated by mastitis. 

Chronic Inflammation of the interstitial connective tissue of the mam- 
mary gland may result in the formation of dense connective tissue (Fig. 
382), with or withotit cystic dilatation of the milk ducts and atrophy of 





Fig. 383.— Chronic Inflaimimation of Mammary Gland. 



the glandular elements. Acute exudative inflammation may occur in 
a gland which is the seat of chronic inflammation, and abscesses may be 
formed. 

Tuberculous Inflammation of the mammary gland and its excretory 
ducts is of occasional occurrence. It may manifest itself in the form of 



THE EEPRODUCTIYE OEGAXS OF THE FE3IALE. 643 

miliary tubercles, larger aud smaller caseous masses of new-formed tissue, 
or cold abscesses. ' 

Syphilitic Ulcers may occur in the nipple either as primary chancres 
or as mucous patches. Gummy tumors have been observed in the 
mamma. 

TUMORS. 

There may be a general hypertrophy of one or both breasts. This is 
usually found in young, unmarried women, but sometimes in women in 






.■»?«.-? 
h^^. 

^'^-^c 



■= 






^1 







'■% 



>.^,-^ :>: 






7 



>.t\t \^ 



::^' I 



Fig. 383.— Ixtracanalicular Fibroma of the Mamma. 

advanced life. There is an increase in both the glandular aud the con- 
nective-tissue elements of the organ. 

Fibroma. — Circumscribed tumors composed of connective tissue are 

' See a bibliograpliic summary of tuberculosis of the breast by Scudder, Am. Jour. 
Med. Sciences, vol. cxvi., p. 75, 1898. 



644 THE REPRODUCTIVE ORGANS OF THE FEMALE. 

sometimes found in the breast. They are dense and hard, and may en- 
close some of the gland ducts and acini. 

Intracanalicular Fibroma. — These tumors are formed by a diffuse 
growth of connective tissue, and a growth of polypoid fibrous tumors 
from the walls of the milk ducts into their cavities leading to dilatation. 



4>^ 






\ ^ „,_ ... :., . ■ _ ... .s^xiMi^:-- -:■ 

Fig. 384.— Intracanalicular Fibro-Adenoma of the Mamma. 
Showing new-formed gland acini in the fibrous-tissue mass growing into a duct. 

The glandular acini may be atrophied, or enlarged, or cystic. A section 
of such a tumor looks like a solid mass of fibrous tissue, divided by clefts 
and fissures lined with cylindrical or cuboidal epithelium (Fig. 383), or 
fibrous tissue containing cysts into which project polypoid fibrous out- 
growths from the walls. Sometimes the new-formed fibrous growths into 
the dilated ducts are adenomatous in character, containing many new- 
formed irregular acini (Fig. 384). Such tumors may be called mtra- 
cancdicular Jibro-adenomata. These tumors grow slowly, but if left to 
themselves may reach an enormous size. The skin over them may ulcer- 
ate and the tumor project through the opening in fungous masses. They 
may be associated with interstitial fibrous hyperplasia of the glaud. 

Fericanalicular Fibroma. — Sometimes the new connective tissue forms 
a more or less thick cylindrical investment of the duct without growing 
into its lumen. This formation, which is shown in Fig. 385, is some- 
times called ijericanalicular fibroma. 

Myxoma. — This form of tumor may occur as a circumscribed growth 
replacing part of the mamma, or it may be developed in the same way 
as the intracanalicular fibromata. It is not uncommon in these intra- 
canalicular tumors to find a combination of fibrous, mucous, and sarcom- 
atous tissue in the same tumor. 



THE EEPHODUCTIYE ORGANS OF THE FEMALE. 



645 



Chondroma is a very rare form, of tumor in the mamma. A few cases 
have been described in which it was combined with carcinoma. 

Adenoma. — Tumors composed of glandular acini and ducts surrounded 
by connective tissue are of frequent occurrence in the mamma (Fig. 
386). They are either single or multiple, or several may be developed 
successively in the same breast. They grow, as a rule, at first slowly, 
afterward more rapidly. Their structure may be further complicated 
by the dilatation of one or more of the ducts which compose the tumor 
into cysts, and the ingrowth of connective tissue from the walls of these 
cysts. This growth is often in papillary f ovm.— jmpiUary cystadenoma — 
(Fig. 387). A case of cystic adenoma with ciliated epithelium has been 
described. ' 

While preserving the gland type the adenomata present great variation 
in the form and grouping of the epithelial cells of the ducts and acini, 
so that here as elsewhere various intermediate forms may be found be- 
tween adenoma and carcinoma. 

Sarcoma. — These tumors may develop in a nodular or diffuse form 
and may largely replace the gland, or may form intracanalicular growths. 
They may be of the round or spindle cell type ; they often become very 
large, and ulcerate. Metastasis in the axillary lymph-nodes is usual. 

Primary Carcinoma of the mamma is most common in women between 
the ages of thirty -five and fifty -five, but it sometimes occurs in women 



'^fKi-r^if^, 




Fig. 385.— Pericanalicular Fibroma of the Mamma. 



not over twenty, and sometimes in old persons. It occurs in either 
breast, in the right rather more frequently than in the left, but some- 
times in both. The growth begins more frequently at the periphery of 

^Buday, Vh-cliow's Arch., Bd. clvi., p. 395, 1899. 



64:(y THE EEPEODUCTIYE ORGANS OF THE FEMALE. 

the gland than at its centre, and more frequently in the upper edge of 
the gland than in any other place. 

The groAvth most frequently begins as a small, circumscribed nodule, 
which enlarges and involves more and more of the breast ; sometimes, 
however, it is diffuse from the first, and sometimes it begins in the nipple. 

It may infiltrate the adjacent tissues and the axillary and cervical 
glands, and form metastatic tumors in different parts of the body. ' 

The local extension of carcinoma often takes place through the lymph - 
vessels which pass along the fibrous trabeculse of the periglandular fat ; 



>;^^ 



>? —^ ,^ , -V. f^i:^''AP^y 












^^^<'^ -"^'-^ °-'- .'-"'' t:^;'^/ ^: 



^,^ 



i1*'>>S-.-iV * 







^s ^^^-^'^^?*^ - %:% j:: 'i . \^ - 

Fig. 386.— Adenoma op the Mamma, 

These new-formed acini while maintaining the gland character are still quite atypical in form and grouping 
and in the irregularity of the epithelium. 

SO that bands of fibrous tissue harboring tumor cells, with their active 
capacity for growth, may extend far from the central mass (Fig. 388). 
Fibrous bands of such significance are, in the early stages of extension, 
not to be differentiated from the normal, either by the touch or by the 
eye. Even with the microscope it is often impossible to determine 
whether small spheroidal or polyhedral cells which are not character- 
istically grouped in these fibrous bands are epithelial in character or not. 
It is such cells, frequently left behind in other than thorough operations, 
which give rise to local recurrence. 

The medullary and fibrous types are most common ; the gelatinous is 
rare. In any of these forms of cancer there may be cystic dilatations of 
the ducts and acini. Epithelioma may form at the nipple. Secondary 

^ For a study of dissemination of carcinoma of the breast see Stiles, Brit. Med. 
Jour., vol. i., p. 1452, 1899. 



THE REPRODUCTIYE ORGANS OF THE FEMALE. 



647 



carcinoma of the mamma is rare. Eetractiou of the nipple is common in 
later stages of fibrons types of mammary cancer (see Fig. 388). 






















"^m: ^ 









Fig. 387.— Papillary Cystadenoma of the Mamma. 

Cysts ot the mamma seem to be for the most part retention cysts, 
formed by the dilatation of the gland ducts or acini. During lacta- 




FiG. 388.— Carcinoma of the Mamma— Fibrous Type— Scirrhus. 

The nipple is retracted by the shrinkage of the fibrous tissue. The growth is extending along the fibrous 
bands of the mammary fat and at the left has reached the plane of excision. The darker portions in the 
figure are lobules of fat. 



648 THE EEPRODUCTIYE ORGANS OF THE FEMALE. 

tion such retention cysts are sometimes formed, and then contain milk. 
They may reach an enormous size. At other times retention cysts are 
formed containing serous or viscid, brownish iiuid, which often exudes 
through the nipple. These cysts may be large or small, single or multi- 
ple. There are usually at the same time some growth and induration of 
the connective tissue of the gland. In some cases there are polypoid 
outgrowths of connective tissue from the wall of the cyst. These cysts 
are not to be confounded with the cysts which are developed with the 
intracanalicular tumors, described above. 



CHAPTER XI. 

REPRODUCTIVE ORGANS OF THE MALE. 

The Penis. 

Malformations . 

The penis may be absent witb great defects of development of the rest of the body. 
The urethra then usually opens into the rectum. 

An abnormally small penis may be associated with absence or arrested develop- 
ment of the testicles. The prepuce may be rudimentary or absent. 

Congenital phimosis is not uncommon. 

Hypospadias is an arrest of development of the penis and scrotum. In its high- 
est degree the penis is short, the glans penis small. On the lower side of the penis is a 
deep cleft lined with mucous membrane. Into this cleft the urethra opens at the root 
of the penis. The scrotum remains separated into two halves, resembling labia majora. 
The testes may descend into their proper position on each side or remain in the abdo- 
men. If the testicles continue to develop normally the individual has the appearance 
and capacities of a man ; if their development is arrested the individual is apt to be of 
feminine type. 

In lesser grades of hypospadias the two halves of the scrotum are joined and the penis 
is larger, but a part of the urethra remains open as a cleft at some point of the penis. 

Epispadias is an opening of the urethra on the upper side of the penis. It pre- 
sents various grades and forms. 

Hermaphroditism. — This is a union of two sexes in the same person, the test of 
which is the presence of the secreting organs, the ovaries and testicles. True hermaph- 
roditism is rare, but it does occur, while most of the conditions called hermaphrodit- 
ism are in reality due to varying malformations of the external generative organs. 

Pseudo-lierma'pJiroditism. — In the male, normally, the greater part of Miiller's canal 
disappears and its lower end forms the vesicula prostatica. In this malformation 
Miiller's canal is changed, as it is in the female, into Fallopian tubes, uterus, and 
vagina, while at the same time the testes, epididymides, vesiculge seminales, and sper- 
matic cord are formed as usual. In the lesser degrees of this malformation we find, in 
the place of the vesicula prostatica, a pear-shaped sac as large as a pigeon's egg, w^ith 
muscular walls and an epithelial lining. This sac may be incompletely divided into a 
uterus and vagina, and it opens into the urethra. In the higher grades we find a well- 
formed vagina and uterus. The uterus may or may not have Fallopian tubes. The 
testicles are usually retained in the abdomen or inguinal canals, and are small. The 
spermatic ducts run on the sides of the uterus and open into the urethra or are closed. 
The penis and scrotum appear as in hypospadias, or are well formed. The appearance 
of the individual varies with the development of the testicles. 

Tnie IIerma2:)7irodit ism msiy he lateral. In this condition there is hypospadias; a 
vagina and uterus and a Fallopian tube and ovary are on one side, and a testicle and 
spermatic cord on the other. 

In certain cases, which may be called bilateral liermapJiroditism, there is a testicle 
on one side and an ovary on the other. ^ 

^ For a detailed consideration of the malformations of the male and female genera- 
tive organs consult Klehs, " Handbuch der pathologischen Anatomic, " and more recent 
cases of hermaphroditism by Heppjier, Arch. f. Anat. u. Physiol., 1870, and by Hof- 
mann, Wien. med. Jahrb., 1877. 



650 EEPRODUCTIYE ORGANS OF THE MALE. 

Enlargement of the Penis is sometimes caused by venous congestion from 
heart disease; by long-continued masturbation, as a result of which the corpus caverno- 
sum may lose its contractility ; and in rare cases by hyperplasia of the stroma of the 
corpus cavernosum. 

INJURY AND HAEMORRHAGE. 

Injuries to the penis are liable to give rise to severe haemorrhage on 
account of its peculiar vascular character ; sui)purative inflammation, 
gangrene, infiltration with urine and its consequences, are also liable to 
occur. The contractions of the cicatricial tissue by which wounds are 
healed frequently give rise to various distortions of the organ. 

INFLAMMATION. 

Balanitis — inflammation of the gians penis and the prepuce — is usually 
due to gonococcal or syphilitic infection, or it may be incited by foul 
accumulations of smegma. The parts are red and swollen and may 
ulcerate. Condylomata may be formed, and adhesions between the pre- 
puce and glans. The glans may ulcerate and the prepuce may be much 
thickened. If the prepuce be long, pliimosis may occur with the accumu- 
lation of exudate beneath. The prepuce may become gangrenous. 

Paraphimosis is produced by the retraction of a narrow prepuce be- 
hind the glans, with consequent stricture, inflammation, and sometimes 
gangrene. 

Inflammation of the Corpora Cavernosa may be the result of injury, may 
follow fistulie, may occur in connection with inflammation of the connec- 
tive tissue of the pelvis, and may accompany the acute infectious dis- 
eases. It may result in fibrous induration of portions of the cori3ora 
cavernosa ; rarely in abscess or diffuse purulent infiltration ; sometimes 
in gangrene. Larger and smaller masses or plates of very dense fibrous 
tissue sometimes form in the sheath of the corpora cavernosa without his- 
tory of antecedent lesion. 

Tuberculous inflammation of the penis has repeatedly followed circum- 
cision performed by uncleanly tuberculous persons. 

Syphilitic Ulcers frequently occur on the glans penis and prepuce. 
The indurated chancre is formed either from an excoriation in which 
a pustule is formed or from a little nodule. The pustule breaks and 
its walls are infiltrated with small round cells. The nodule softens, 
breaks down, and forms an ulcer whose walls are infiltrated with cells. 
Syphilitic condylomata are of frequent occurrence on the glans. 

Herpes of the prepuce occurs in the form of small vesicles, which may 
later become ulcers. Erysipelatous and furuncular inflammation some- 
times involves the skin of the penis. 

TUMORS. 

Papilloma is found on the prepuce and glans penis. It occurs in the 
form of little warty growths, or of composite, cauliflower masses, even 
as large as a fist. In either case the structure is the same — hypertro- 



REPRODUCTIVE ORaANS OF THE MALE. 651 

phied papillae covered with epithelium. Sometimes the epithelial layers 
become thick and hornj^, forming large, dense projections. 

Fibroma diffusum, or elephantiasis of the prex^nce, may occur, leading 
to great thickening. It is due to a diffuse growth of fibrous tissue in the 
cutis. Lipoma, angioma, circumscribed fibroma, and sebaceous cysts may oc- 
cur in the penis. Carcinoma is usually of the epitheliomatous type. It 
is most frequent in the prepuce and gians penis. It may have the form 
of a flat ulcer, or of infiltrating, ulcerating nodules, or it may be papil- 
lary. Such growths may attain great size, ulcerate, or undergo a variety 
of inflammatory changes. Carcinoma may involve the entire skin of the 
penis or may invade deeper j)arts. The inguinal glands may be involved. 
Distant metastases are not frequent. 

Medullary or glandular carcinoma of the penis is not common. It 
may be secondary to carcinoma in some other part of the body. 

Dermoid tumors of the penis are of occasional occurrence. ' 

Calcification and Ossification of the connective tissue of the corpora 
cavernosa sometimes occur. Large and small preputial calculi are occa- 
sionally found between the prepuce and the glans. These may be formed 
in situ, may come from the bladder or from without, and may later in- 
crease in size. 

The Scrotum. 

The skin of the scrotum is subject to the various forms of lesions 
which may occur in any part of the integument. 

Elephantiasis of the scrotum consists in the main of a development of 
new connective tissue in the cutis, which is sometimes accompanied by 
dilatation of the lymph- vessels ; thus the thickened scrotum may form a 
large tumor, often rough upon the surface, which may entirely cover in 
the penis. 

TUMORS. 

Lipoma and fibroma occur. Epitheliomata, in the form of flat or 
papillary ulcerating tumors, are of frequent occurrence among chimney 
sweepers, and may lead to extensive ulcerations of the adjacent parts and 
involvement of neighboring lymph-nodes. 

Dermoid Cysts and Teratomata of the scrotum are not uncommon. In 
very rare cases tumors containing a considerable portion of a foetal skele- 
ton have been found in the scrotum. Occasionally the skin of the scrotum 
is beset with numerous larger and smaller sebaceous cysts, which raise 
the surface into little globular or wart-like projections. 

The Testicles. 

Malformations . 

Absence of both testicles, either with or without absence of the epididymides, 
spermatic cords, and vesiculge seminales, occurs in rare cases. The scrotum is only indi- 

1 Gerulanos, Deut. Zeits. f. Chir., Bd. Iv., p. 326. 



652 REPRODUCTIVE ORGANS OF THE MALE. 

cated or may contain the epididymides. The penis is small, and the individuals are 
small and poorly developed. 

The testes may be imperfectly developed. The individuals are effeminate. Ab- 
sence of one testicle, with healthy development of the other, is more frequent. The 
corresponding epididymis and cord may be absent or present. 

The spermatic cords and vesiculce seminales may be absent or imperfectly devel- 
oped on one or both sides, while the testes are normal. 

Cryptorchtsmus.— Either one or both testicles may remain permanently in their 
foetal position, or may not descend into the scrotum for several years after birth (cryptor- 
chismus), or not at all. This condition may be due to an arrest of development in the 
testes or the gubernaculum testis; adhesions produced by antenatal peritonitis; nar- 
rowing of the inguinal canal; narrowing or shortening of the vaginal process of the 
peritoneum ; or to abnormal size or position of the testicle. Usually the malformation 
is confined to one testicle, and then is more frequent on the left side. The testicle is 
usually found in the abdomen close to the mouth of the inguinal canal, or in the ingui- 
nal canal just below the external ring; but it may be beneath the skin in the perineum, 
or in the crural canal with the femoral vessels, or elsewhere. The retained testis is 
usually not fully developed, or undergoes fatty degeneration or fibrous hyperplasia. 
The retention of one or even of both testicles does not preclude the possibility of pro- 
creation. Retained testicles are prone to inflammatory changes and liable to become the 
seat of malignant tumors. 

Sometimes, while the testis is retained, the epididymis and spermatic cord descend 
into the scrotum. In rare cases the position of the testis may be changed so that the 
epididymis and cord are in front. The existence of a supernumerary testis has been 
asserted. 

Hydrocele. 

In hydrocele of the tunica vaginalis there is an accumulation of fluid in the cavityof the 
sac. It is usually unilateral and is usually associated with acute or chronic inflammation 
of the tunica vaginalis, varicocele, or general dropsy. The serum is present in small or 
in large quantit}- ; it is usually transparent, may contain cholesterin, or be purulent or 
mixed with blood. The tunica vaginalis remains unchanged, or is thickened, or con- 
tains plates of bone, oris covered with polypoid fibrous bodies which may fall off and be 
found free in the cavity of the sac. There may be adhesions between the layers of the 
tunica vaginalis, and in this way the fluid becomes sacculated. The testis is pushed 
downward and backward; it remains unchanged or is atrophied. 

In liydrocele of the processus vaginalis there is an accumulation of serum in the 
cavity of the vaginal process of the peritoneum, which remains open after the descent 
of the testicle. There are several varieties. 

{a) The vaginal process is entirely open and there is a free communication with the 
peritoneal cavit3\ The serum may originate in the cavity of the peritoneum or of the 
vaginal process, and passes freely from one to the other. 

{b) The processus vaginalis is closed in the inguinal canal, w^hile its lower portion 
is filled with serum. 

(c) The processus vaginalis is closed about the testis and the visceral layer of the 
tunica vaginalis is formed. The serum accumulates in the upper part of the vaginal 
process which communicates with the peritoneal cavity. 

{d) The vaginal process is closed in the inguinal canal and over the testis ; the serum 
accumulates so as to form one or more sacs between these two points. Inguinal hernia 
may complicate this form of hydrocele. 

In liydrocele of the spermatic cord there is general oedema or the development of cir- 
cumscribed cysts in the connective tissue of the cord. 

A peculiar type of hydrocele is formed by the accumulation of serum in the sac of 
an inguinal hernia from which the intestine has become retracted. 



KEPRODUCTIYE ORGANS OF THE MALE. 653 



Haematocele. 

In haematocele of the tunica vaginalis there is an effusion of blood into the cavity 
of this sac. It may occur in injury; in scurvy, or with the hsemorrhagic diathesis; or 
it may complicate a pre-existing hydrocele. The effused blood usually soon degen- 
erates, and the sac is filled with a brownish fluid or a thick, grumous mass. The tunica 
vaginalis may be thickened. The testis remains normal or is atrophied. 

Effusion of blood into the loose connective tissue of the scrotum is often called 
extvavaginal hcematocele. 

Hoematocele of the spermatic cord occurs in rare cases as a diffuse infiltration of 
blood in the connective tissue of the cord. Or blood may be effused into a hydrocele of 
the cord. 

Spermatocele. 

Cysts containing spermatic fluid not infrequently arise from the epididymis or 
from the rete testis. These sometimes acquire a large size and crowd the tunica vag- 
inalis before them, so that they simulate a collection of fluid in the cavity of the latter. 
The wall of the cyst may be lined with ciliated or with flattened epithelium. The 
contents are sometimes simply serous, but more frequently opalescent, and may contain 
spermatozoa. 

ATROPHY. 

Atrophy of the testicle may occur in old age or in persons who are in 
a condition of premature senility ; or as the result of pressure from her- 
nise, hydrocele, or inflammatory products. 

INFLAMMATION. (Orchitis.) 

Inflammation of the testicles may follow injuries, exposure to cold, and 
inflammation of the urethra ; it may occur in parotitis or with syphilis 
and various other infectious diseases. The testes, epididymis, or tunica 
albuginea may be principally involved. Usually only one testicle is in- 
flamed, sometimes both. The inflammation may extend to the vas def- 
erens. 

Acute Exudative Orchitis is most frequent in the epididymis and tunica 
albuginea. AATien the testis is involved the organ is congested and in- 
filtrated with serum or pus. From this condition it may return to the 
normal state ; or small abscesses may form which may be absorbed, or 
increase in size so as to involve nearly the entire organ. They may 
perforate externally, and then healing may occur by means of granula- 
tion tissue; or extensive gangrenous destruction of the scrotum may 
occur. Abscesses may become enclosed in a fibrous capsule, when the 
contents may dry and become caseous or calcified, and so persist for a 
long time. The acute inflammation may become chronic. 

Acute epididymitis is frequently the result of gonorrhoeal infection, 
and may or may not be associated with inflammation of the testis. The 
products of inflammation may collect in varying quantity in the lumina 
of the seminiferous tubules and in the ducts of the epididymis, and the 
epithelium of these structures may degenerate. 



654 



REPRODUCTIVE ORGANS OF THE MALE. 



Chronic Orchitis occurs as a sequel of acute inflammation or as an in- 
dependent process. It may involve the testis, the epididymis, or the 
spermatic cord. The seminiferous tubules may be filled with desqua- 
mated and degenerated epithelium ; they may be atrophied, or their walls 



a. 






mxi'^PHA 













Fig. 389.— Chronic Interstitial Orchitis with Atrophy of the Seminiferous Tubules. 

a. Thickened interstitial tissue ; c, thickened membrana propria of the tubules ; d, separated epithelial cell 

mass in the lumen of the tubules. 



may be greatly thickened so that they are converted into dense fibrous 
cords, with partial or complete obliteration of their lumina. There is 
usually a marked increase in the interstitial tissue, which causes atrophy 
of the tubules (Fig. 389). Thealbuginea maybe greatly thickened. In 
some cases the testis is converted into a mass of dense fibrous tissue, in 
which but little trace of the original structure can be made out. The 
new -formed fibrous tissue may become calcified. A periorchitis may 
lead to thickening and union of the layers of the tunica vaginalis testis. 
Abscesses are not infrequent in connection with chronic orchitis. 

Tuberculous Orchitis may occur in connection with tuberculosis of the 
other genito -urinary organs or the lungs, in acute general miliary tuber- 
culosis, or independently. It usually originates in the epididymis, and 
may extend from there to the testis ; or it may commence in the testis. 
The appearances which the testicles present, when they are the seat of 
this form of inflammation, are exceedingly varied and often difficult of 
inter]3retation. This is partly due to the complex structure of the organ, 
partly to the varied complicating simple inflammatory changes which 
the different parts of the organ undergo in connection with the tuber- 
culous lesion. 

We may find in the testicle small circumscribed masses of cells, visi- 
ble to the naked eye as whitish spots, which are sometimes composed of 
small spheroidal cells or of larger polyhedral or fusiform or round cells. 
These occur in the walls of seminiferous tubules and blood-vessels, and 



EEPUODUCTIYE ORGANS OF THE MALE. 655 

iu the interstitial tissue. Sometimes associated vrith these smaller nod- 
ules, and sometimes not, we find larger, irregular yellowish or gray 
cheesy masses, which may be formed by the confluence and degeneration 
of the smaller nodules. The cheesy masses may break down and open 
externally, giving rise to fistulse, gangrenous inflammation, etc. 

Hand-in-hand with this distinctly tuberculous nodular formation of 
tissue, which is disposed to degenerative changes, there are various more 
or less diffuse alterations of the parenchyma and interstitial tissue of 
the organ which often constitute a most j)rominent feature of the lesion. 
The interstitial tissue may be more or less densely and diffusely in- 
filtrated with small spheroidal cells. The arteries are often the seat of 
obliterating endarteritis. The walls of the seminiferous tubules may be 
very much thickened, so that the lumen may be entirely obliterated. 
The epithelium lining the tubules may be fatty, disintegrated, and peeled 
off, or it may have largely disappeared. The lumen of the tubules may 
be filled with a granular, nucleated mass which in transverse sections 
looks like a giant cell. The thickened walls of the tubules may be in- 
filtrated with small spheroidal cells, so that the underlying stroma is 
scarcely visible. When this occurs in connection with a similar infiltra- 
tion of the interstitial tissue and the formation of giant cells in the lumina, 
we have structures which present the greatest resemblance to some forms 
of tubercle granula (Fig. 390). 

Tuberculous inflammation may extend from the testis to the vast def- 
erens, vesiculae seminales, and prostate. 

Syphilitic Orchitis. — This may occur in the form of a diffuse new forma- 
tion of connective tissue, which may be localized or be widely distributed. 




Fig. 390.— Chronic Orchitis tvith the Formation of Structures Resembling Miliary Tubercles. 

a. Thickened interstitial tissue ; 7:>, mass of granular cells in the Interstitial tissue ; c, thickened mem- 
brana propria of seminiferous tubule ; c7, mass of separated epithelium in tubule ; e, accumulation of small 
spheroidal cells around tubules ; /, thickened membrana propria enclosing g, a multinuclear mass resem- 
bling a giant cell. 

This organ becomes dense and firm. Morphologically there is no differ- 
ence between this form of orchitis and chronic indurative orchitis from 
other excitants. It may occur in children affected with, congenital 



656 REPRODUCTIVE ORGANS OF THE MALE. 

syphilis. Gummata may form in connection with the interstitial indura- 
tion. These may disappear, leaving irregular cicatrices. 

In leprosy, inflammatory foci in the testicle are common.^ - 

TUMORS. 

Fibromata occur in the form of small dendritic or polypoid growths of 
the visceral layer of the tunica vaginalis. These sometimes become free 
and are found in the sac, usually in connection with hydrocele. Small 
nodular fibromata occasionally occur in the albuginea and in the sper- 
matic cord. 

Lipoma, either pure or in combination with myxoma and sarcoma, 
may arise from the connective tissue of the spermatic cord or from the 
tunica albuginea. 

Chondroma, sometimes in a pure form, but more frequently combined 
with myxoma and sarcoma, occurs in the testicles and may attain a large 
size. Osteoma has been described. 

Sarcomata occur in the testes and epididymis, most frequently in the 
former. They may be composed of spheroidal or spindle-shaped cells; 
they may be soft or contain much fibrous tissue ; they are very frequently 
combined with myxoma, chondroma, lipoma, etc. Owing to the occlu- 
sion of the seminiferous tubules, cysts may be formed in these sarcomata. 
In such cysts sarcomatous tissue may occur in the form of intracanalic- 
ular polypoid growths. Thus the so-called ci/sto-sarco7nata of the testi- 
cle are formed. The walls of these cysts may coalesce, so that large, 
irregular cavities may be formed. When the cysts are not filled by 
polypoid outgrowths from their walls they may contain a mucous, serous, 
or bloody fluid, or masses of flattened cells, fat, and cholesterin. The 
cysts may be lined with cylindrical, ciliated, or flattened cells. 

Rhabdomyoma has been several times observed, frequently in com- 
bination with cysts. ^ 

Adenoma is occasionally found, usually in combination with sarcoma 
or carcinoma, or with cyst formation. 

Carcinoma of the testicle is commonly of the soft medullary form, of 
rapid growth, and usually primary. It may commence in the testis or 
epididymis. Usually only one testicle is involved. Frequently the en- 
tire glandular iDortion of the organs is replaced by the new growth. The 
albuginea expands with the growth of the tumor, and may continue to 
enclose it even when of large size. The tissues are often very vascular, 
and haemorrhages, areas of softening, fatty and mucous degeneration are 
frequent. The inguinal and lumbar lynij)h-nodes are apt to become in- 
volved, and distant metastasis may occu.r. Earely the growth assumes a 
scirrhous form. 

Cysts. — Aside from the above-mentioned cysts which occur in connec- 

^ For a summary of orchitis, with bibliography, consult Sehileau, Arch. gen. de 
med., t. i., pp. 636, 757, 1899. 

-For study of rhabdomyoma, with bibliography, see Becker, Yirchow's Arch., Bd. 
clxiii., p. 244, 1901. 



REPRODUCTIVE ORGANS OF THE MALE. 657 

tion with tumors and spermatocele, cysts may be formed from persistent 
remnants of Miiller's canal in the epididymis, or from obstruction of the 
seminiferous tubules or ducts by inflammatory products or tissue. 

Teratoid tumors of various kinds, with or without cysts, are of infre- 
quent occurrence, and are sometimes quite complex in character. They 
may be embedded in the substance of the gland. ' Probably some of the 
above-mentioned cystic rhabdomyomata belong here. 

PARASITES. 
Echinococcus may occur in the testis or epididymis. 

The Seminal Vesicles. 

The seminal vesicles may be the seat of acute or chronic inflammation, 
which is most frequently connected with inflammatory changes in ad- 
jacent parts, i)rostate, urethra, etc. As a result of chronic inflammation 
the vesicles may be atrophied, or they may be greatly dilated, forming 
cysts due to constriction of the ducts. Tuberculous inflammation is usu- 
ally secondary. 

TUMORS. 

Carcinoma of the rectum or other genito-urinary organs may secon- 
darily involve the seminal vesicles. Small concretions, sometimes con- 
taining masses of spermatozoa, are occasionally found in the seminal 
vesicles. 

The Prostate. 

DEGENERATION, ATROPHY, AND HYPERTROPHY. 

Fatty and hyaline degeneration of the muscle may occur in the pi'ostate 
with or without hypertroi^hy. Atrophy of the prostate may follow lesions 
or removal of the testicle, inflammation of the prostate itself, and may 
occur as a senile process. Dilatation of the ducts may accompany the 
atroi:)hic process. 

Hypertrophy. — Enlargement of the prostate— so-called hypertrophy — 
is of frequent occurrence in advanced years. It may involve the entire 
organ or be partial ; it may be noduiar or diffuse. The middle lobe is 
most frequently involved, and this may press ux)on the urethra, leading 
to difficult urination and such secondary alterations in the bladder as are 
associated with this, i.e., hypertrophy and dilatation of the bladder, oi 
cystitis, not infrequently with involvement of the ureter and kidneys. 

Hyi^ertrophy of the prostate may be due to hyi^erplasia of the mus- 
cle and fibrous tissue of the organ ; at the same time the gland tissue may 
be increased (Fig. 391), or the latter may be alone involved. The in- 
crease in gland tissue has usually the character of glandular hyioerx^lasia. 

' Consult for teratoid tumors of the testicle TF«7//ii.s, Ziegler's Beitr. z. path. Anat.; 
Bd. xix.. p. 233. 1896. 
42 



658 



REPRODUCTIVE ORGANS OF THE MALE. 



But genuine adenomata may form both with and without hyperplasia of 
the connective tissue, muscle, and glands. 

In partial hypertrophy there are circumscribed nodules of muscle 
tissue or of muscle and gland tissue. These are usually situated at the 






^^ -^ -^.-c >w \k.^ 




Fig. 391.— "Hypertrophy"— Hyperplasia— of the Prostate. 
There is glandular hyperplasia as well as hyperplasia of the flbro-muscular stroma. 

periphery of the organ and i)roject into the bladder. They may become 
detached from the prostate, and found as small, movable tumors beneath 
the mucous membrane of the bladder. 



INFLAMMATION. (Prostatitis.) 

Acute exudative inflammation of the iDrostate is induced by gonorrhoea, 
by injuries, or, more rarely, is independent. It maybe acute or chronic. 
The gland may after a time return to its normal condition, or is gradu- 
ally converted into a mass of fibrous tissue filled with abscesses. The 
abscesses may perforate into the bladder, urethra, vesiculse seminales, 
rectum, or peritoneum. Or the inflammation may extend to the connec- 
tive tissue of the scrotum or beneath the pelvic peritoneum. The pus 
may become thickened and cheesy, or even calcified. 

Tuberculous Inflammation of the prostate usually accompanies a similar 
lesion of some of the other genito-urinary organs. Large cheesy masses 
are often formed, which may break down and open into the bladder or 
rectum. 



REPRODUCTIVE ORGANS OF THE MALE. 659 



TUMORS. 

Sarcoma of the prostate has been described. Adenoma (Fig. 392) 
occurs either with or without an increase in the fibro-muscular interstitial 
tissue and gland hyperx)lasia. 

Carcinoma is of occasional occurrence, and may be primary or secon- 
dary. 

Cysts of the prostate are sometimes found either as a result of occlu- 



- , VE^ . 


- K ■^i^-f-—'- ^jr-*- „-<^-?- 






^ 


"■ 




^ 


ii-~ 




f/-'^ 


N 


j.- 


«. "^ * 




-c 


^ 


^ . V. 


^„ 




/ 


"V-j.. 






^ 


■"^h.ir-'- 


.-^- .:. ^ ^'^ ^ ' 







Fig. 392.— Adf.xoma 07 thk Prostate. 

In the upper portion of the cut, at ihe liRht, are three nearly normal acini of the prostate, while the re- 
mainder shows various phases of new gland formation. The prostate, in addition to the circumscribed 
tumor growth, was the seat of the usual glandular and interstitial hyperplasia. 

sion of the ducts by hyi^ertrophy of the interstitial tissue, tumors, etc., or 
as a result of faulty development. 

PARASITES AND CONCRETIONS. 

Echinococcus of the prostate has been described, but is rare. 

Concretions. — Small ovoidal or spheroidal, often brown or black bodies, 
having the characters of corpora amylacea, are of very frequent occur- 
rence in the alveoli of the prostate, particularly in old persons. We find 
a certain number of them in the prostate of nearly all old men, but they 
aie sometimes present in great numbers. Larger, irregular concretions, 
apparently formed by the coalescence or growth of the smaller ones, are 
less frequently found, and may be encrusted with lime salts. These con- 
cretions may give rise to ulceration of the ducts of the gland or to inter- 
ference with the passage of urine, but usually they are of no practical 
importance. 

Cowper's Glands. 

Inflammatory ijrocesses, acute or chronic, may occur in these organs in 
connection with urethritis or prostatitis. Abscesses may form; the 
glands, either in acute or chronic inflammation, may become enlarged 



660 REPRODUCTIVE ORGANS OF THE MALE. 

and encroacli upon the lumen of the urethra. Retention cysts formed by 
the closure of the excretory ducts may also project into the urethral 
canal. 

The Male Mamma. 

There may be an abnormal number of mammae. In boys, at about 
the time of puberty, the mammae may be swollen and inflamed or they 
may secrete milk. Cases are recorded in which adult males possessed 
large mammae which secreted milk. The breasts may be enlarged from 
an increase of fat or of connective tissue. 

Fibroma, sarcoma, cysto-sarcoma, myxoma, and various forms of carci- 
noma may occur. 

Cysts of the male breast are not very infrequent. 



CHAPTER XII. 

THE BONES AND JOINTS. 
The Bones. 

ATROPHY. 

I:n^ old age or in senile conditions the bones may become atrophied by 
the absorption of the hard tissue ; the medullary spaces are enlarged, the 
marrow tissue contains less fat and is often gelatinous in appearance. 
As the result of the lack of use, or from any cause which interferes with 
the nutrition of the bone, such as paralysis of the muscles or diseases of 
the joints, the bones may atrophy. In connection with atrophy there 
may be an ossifying periostitis, which results in making the bone look 
even larger than normal. Many of the conditions common] y called 
atrophy, such as the erosions of bones from tumors, etc. , pressing upon 
them, are really due to a rarefying osteitis. 

The bones, sometimes as the result of atrophy and sometimes from 
causes which we do not understand, are unusually brittle and liable to 
fracture. This disposition is sometimes hereditary. 

DISTURBANCES OF CIRCULATION. 

Hyperaemia. — The evidences of this condition are most marked to the 
naked eye in the periosteum and marrow, particularly the latter. It 
should be remembered that the color of the marrow varies considerably 
under normal conditions, depending upon age and situation. In the 
bones of the foetus and new-born, and near the areas of ossification in the 
young, the marrow is normally red in color. In adults the marrow of 
the sternum, vertebrae, and to a certain degree that of the ribs, pelvic 
and cranial bones, and the cancellous tissue of the ends of the long bones, 
is red or reddish in color. But most of the marrow, particularly in long 
bones of the extremities, is of a yellowish color from the presence of fat 
cells. In old age the marrow of all the bones is apt to become pale, and 
to assume a more or less translucent or gelatinous appearance. 

Hyperaemia usually occurs as an accompaniment of inflammatory proc- 
esses in the bone, and, when marked, the periosteum is swollen and red ; 
the compact bone tissue may appear of a pink color, while the marrow, 
either by an increase in the amount of blood or absorption of its fat, or 
both, may be of a uniform dark -red color or mottled with red and red- 
dish-yellow. 

Haemorrhage. — This may be due to wounds and injuries, to inflamma- 
tory and necrotic processes; and small haemorrhages often accompany 



662 THE BONES AND JOINTS. 

scurvy, purpura, hsemorrhagic diathesis, and leukaemia. Clots of con- 
siderable size between the periosteum and bone may lead to serious con- 
sequences, by cutting off the blood supply to the superficial layers of 
bone and thus inducing necrosis ; but when not liable to bacterial con- 
tamination through contact with the air they are not usually of serious 
import, and are readily absorbed. The smaller haemorrhages of the 
medulla are not usually of much importance. The decomposition of the 
extravasated blood may lead to extensive pigmentation of the marrow. 

HEALING OF WOUNDS AND FRACTURES OF BONE. 

The process of healing in bone after fracture is, when uncomplicated, 
at first similar to that in ordinary healing by second intention in fibrous 






• ( \ 









^> 











<»- ft- 



Fig. 393.— New-Formed Cartilage and Osteoid Tissue from Callus after Fracture of the Femur. 

tissue. The blood and other exudates and the tissue detritus are gradu- 
ally absorbed or disposed of by phagocytes. By a proliferation of con- 
nective-tissue cells of the region a larger or smaller mass of granulation 
tissue is formed. This granulation tissue does not at first differ in 
appearance from similar tissue formed elsewhere in the body in the 
reparative phase of exudative inflammation. 

But soon, under the influence of the specially endowed cells of car- 
tilage or bone or periosteum, but especially of the latter, the granulation 
tissue becomes partially replaced either by cartilage, or by a substance 
resembling bone in general appearance, but containing no lime salts. 
This is called osteoid tissue. These new cartilaginous and osteoid tissues, 
which are apt to occur together, form irregular masses or interlacing 



THE BONES AND JOINTS. 663 

trabeculse iu the stroma of granulation tissue. This constitutes the 
so-called callus of a uniting fracture (Fig. 393). 

Gradually the osteoid tissue becomes osseous, and the masses of car- 
tilage and bands of periosteal and other fibrous tissue, under transform- 
ations practically identical with those seen in normal development, are 
converted into bone. Thus by gradual absorption and re-formation of 
bone in the usually redundant provisional bony mass, and by the readjust- 
ment of its vascular channels, the healing, with more or less permanent 
deformity, is accomplished. 

If the conditions be not favorable, the healing of fractures may occur 
only by fibrous-tissue formation, so that so-called ^' false joints " may 
result. The healing of other injuries and losses of substance occurs by 
a process similar to that described in fractures. 

INFLAMMATION. 

The periosteum, bone tissue, and marrow are so intimately connected 
that in most cases they all share to a greater or less degree in the patho- 
logical alterations of the bones. But as sometimes one, sometimes another 
is most markedly involved, it is convenient to consider separately here 
the inflammatory changes by which they are respectively affected. 

Periostitis. 

We may distinguish several forms of periosteal inflammation. 

Simple Exudative Periostitis.— Thi^ is apt to occur in children and ill- 
nourished persons after comparatively slight injuries or from unknown 
causes. The iDeriosteum is thickened, succulent, congested, and more or 
less abundantly infiltrated with leucocytes. The periosteum becomes 
less firmly adherent to the bone, and the cells of the inner layers are 
increased in number. This form of inflammation may terminate in 
resolution, or it may lead to other phases of inflammation. 

Suppurative Periostitis may begin as a simple or as a purulent inflam- 
mation. The pus is formed in the inner layers of the periosteum, and 
between it and the bone. The outer layers of the periosteum may for a 
long time resist the suppurative process. The accumulation of pus may 
dissect up the membrane from the bone and leave the latter bare. The 
pus thus formed may remain in this position for a long time, or be 
absorbed, or become dry and cheesy, or it may burst through the perios- 
teum and lead to abscesses in the soft parts. The bone, if separated from 
its nutrient membrane, may remain unchanged, but more frequently 
necrosis or inflammation of the bone itself is set up. Such a periostitis 
may run an acute or a chronic course. 

Sometimes suppurative periostitis takes on a very malignant char- 
acter. Pus is developed not only beneath, but in the periosteum, forming 
abscesses filled with foul pus. The periosteum breaks down into a gan- 
grenous, foul-smelling mass, and the same change may affect the neigh- 
boring soft parts. The medulla may take part in the process and break 



664 



THE BONES AND JOINTS. 



down into a purulent, gangrenous mass. Hgemorrhages may complicate 
the process. The lymph-nodes are enlarged and swollen ; abscesses may 
form in different parts of the body, and the patient may die with the 




Fig. 394.— Ossifying Periostitis— Tibia. 
Large exostoses at the end of the bone. The process involves the joint and the bone is enlarged. 

symptoms of pysemia. The Streptococcus and Staphylococcus pyogenes 
are the most common excitants of suppurative inflammation. 

Fibrous Periostitis. — This is a chronic form of inflammation, resulting 
in the development of new connective tissue in the i)eriosteum, which 
becomes thickened and dense and unusually adherent to the bone. It 
may accompany necrosis, chronic arthritis, chronic ulcers of adjacent soft 
parts, etc., or follow simple acute periostitis. 

Ossifying Periostitis results in the formation of new bone from the inner 
layers of the periosteum. The masses of new-formed bone, called osteo- 
phytes, are of variable shape. They may form a thin, velvet-like, villous 




Fig. 395.— Ossifying Periostitis aA'Ith Large Exostoses— Femur. 

A large part of the shaft is thickened and covered with ragged platelets of new-formed bone, while above 
large rough exostoses project. This bone has been the seat of rarefying and formative osteitis. 



layer; or they are little spicula; or they form larger, rounded masses 
(see Figs. 394 and 395), or a thick, uniform layer extending over a large 
part of a bone. They may have at first a loose, spongy character, and 
be loosely connected with the old bone. But layers of compact bone 



THE BONES AXD JOINTS. 665 

tissue are formed within their medullary spaces, which are thus gradually 
filled, and they join the old bone so that they may finally become as 
compact as or even more compact and dense than normal bone to which 
they are firmly joined. The hyperostoses and exostoses thus formed may 
remain indefinitely, or they may gradually become smaller and finally 
disappear by absorption. 

The formation of new bone in osteophytes, or in dense masses beneath 
and in the periosteum, occurs as a result of the same process by which 
bone tissue is normally formed. Certain large cells, called osteoblasts, 
which are developed along the blood-vessels, possess the power of deposit- 
ing osseous basement substance about themselves and so forming bone. 
Pathological new formation of bone differs from the normal mainly in the 
conditions under which it occurs. The blood-vessels around which the 
pathological bone develops, which grow out of the old vessels, as in the 
formation of granulation tissue, are irregularly arranged and subject to 
a variety of abnormal nutritive and mechanical conditions, so that the 
new bone is usually formed, not in a series of definite systems of lamellae, 
but, as above described, in a series of irregular spicula or masses. More- 
over, as will be seen further on, the conditions under which it is formed 
being liable to change, and itself serving no definite purpose in the 
economy, as does normal bone, pathological new bone is often an evan- 
escent structure. The details of its disappearance will be considered 
below. 

Syphilitic Periostitis. — Syphilitic infection may excite simple, purulent, 
fibrous, or ossifying periostitis. In addition to these, gummy tumors 
may be developed in the periosteum. The bone tissue is usually more or 
less involved. The gummata may be absorbed or undergo cheesy degen- 
eration, or be converted into fibrous tissue, or they may suppurate. 

Tuberculous Periostitis. — In badly nourished persons, particularly in 
children suffering from scrofula, chronic purulent periostitis is frequently 
associated with the formation of miliary tubercles. Abscesses are apt to 
form in and about the periosteum, and when these are evacuated granu- 
lation tissue may develop, which contains miliary tubercles. The bone 
is apt to be involved to a greater or less extent in simple inflammatory 
changes or caries. 

Osteitis. 

Inflammation in bone tissue is dependent upon the same general con- 
ditions and presents essentially the same series of phenomena as inflam- 
mation in other kinds of connective tissue. But it is variously modified 
in detail by the peculiar dense and unyielding character of the basement 
substance, and by certain peculiarities of the blood supply and the 
nutritive conditions under which the cells are placed. In simple exuda- 
tive inflammation the same series of phenomena occur in connection with 
the blood-vessels as in other tissues, resulting in the i^roduction of serum, 
fibrin, and pus; but the extent to which these changes occur is lim- 
ited and constantly associated with striking alterations in the basement 



666 THE BONES AND JOINTS. 

substance. It is these secondary alterations in the basement substance 
which lend to inflammations of the bone their most peculiar characters, 
and in the prominence which these assume the fundamental alterations 
are often overlooked. The most common of these secondary alter- 
ations are the absorption of the hard basement substance of the bone and 
its replacement by, or conversion into, young cellular forms of fibrillar 
connective tissue or marrow tissue, and the new formation, in a more or 
less typical manner, of new bone. As a result of these changes the bone 
in simple inflammation becomes more vascular, and, with an increase of 
spaces filled with granulation or marrow tissue, more porous at the 
expense of the dense basement substance. Or the new-formed spaces 
or the marroAv cavities may be constantly encroached upon by the new- 
formed bone lamellse on their walls, so that the bone becomes more com- 
pact. Or, as is frequently the case, both series of changes occur either 
simultaneously in different regions, or follow each other, or are vari- 
ously associated together. Very frequently one or the other of the oppos- 
ing forms of alteration predominates, or one may occur to the exclusion 
of the other, and we thus have two prominent forms of inflammation, 
which are called rarefijlng osteitis or osteo-jwrosis, and condensiyig osteitis or 
osteosclerosis. The exact nature of the conditions under which in one 
case the bones become more, in another less dense, we do not understand. 
Furthermore, more or less characteristic forms of inflammation may occur 
in syphilitic and tuberculous infection — syphilitic and tuberculous osteitis. 
Suppurative osteitis may further complicate the process. 

In addition to these phases of inflammation in bone, and in frequent 
and varied association with them, there are alterations leading to death 
and destruction of bone tissue in greater or less amount, which are called 
caries and necrosis. Finally, any of these forms, and commonly several 
of them at once, are variously associated with more or less marked 
inflammatory or degenerative alterations of the periosteum on the one 
hand, or the marrow tissue on the other, or of both combined. 

Rarefying Osteitis consists essentially in the formation in the marrow 
spaces. Haversian canals, or beneath the periosteum, of new, very cel- 
lular and vascular tissue, resembling granulation or young marrow tissue, 
under whose influence the basement substance of the bone is absorbed, 
This absorption of the bone takes place largely as bone is absorbed in 
normal growth, namely, under the influence of certain large cells, which 
are grouped around the blood-vessels. If a thin section of bone which 
is undergoing absorption be examined (Fig. 396), the edges of the bone 
which border on the vascular surfaces are found irregularly indented by 
deep or shallow depressions, sometimes simple, sometimes quite complex. 
These are called Hoivship's lacunce and are usually filled or lined by larger 
and smaller granular, frequently multinuclear cells — the so-called osteo- 
clasts. In the larger lacunae there may be granulation tissue with loops of 
blood-vessels, with or without osteoclasts. Under the inflAience of the 
osteoclasts or of the new vascular tissue, the bone is gradually ab- 
sorbed. 



THE BOXES AXD JOINTS. 667 

On the other hand, there may be irregular branching channels through 
the bone across the lamellae, which appear to be due to the enlargement 
and coalescence of the lacunae and canaliculi, without the direct influence 
of blood-vessels or other cells than the fixed cells of the bone. 

The tissue which replaces the absorbed bone may be very rich in 
small spheroidal cells, or it may be more or less fibrillar. 

As a result of this process irregular islets of bone tissue may be 
entirely separated from adjacent bone and surrounded by a more or less 




Fig. 396.— Rarefying Osteitis in Ulna of Child. 
a, Isolated bone fragmeut with rough edges ; b, marrow tissue ; c, Howship's lacunee with osteoclasts. 

fibrillar vascular tissue ; this is most apt to occur in the cancellous tissue. 
Or the originally compact bone may become traversed by a series of larger 
and smaller irregular branching, communicating channels with ragged 
walls. These progressive alterations may cease, and be succeeded by a 
new formation of bone along the edges of the channels or cavities. 

Earefj'ing osteitis may occur as an independent process from unknown 
causes; it is often associated with scrofula, with diseases of the joints, 
with fractures or other injuries to the bone ; it often forms a iDredominant 
feature in tuberculous inflammation of the bones. It is chiefly by a 
rarefying osteitis that bone tissue is eroded and destroyed in the vicinity 
of tumors, aneurisms, etc. , which exert pressure on the bones. By the 
same process the sharj) ends of fractured bone may be rounded off as 
healing proceeds. 

^Vhen this form of inflammation occurs in cancellous bone tissue the 
marrow is red or gelatinous, and the bony septa may disappear altogether, 
so that in extreme cases there may be, instead of cancellous bone, a mass 
of granulation tissue. AMien the process occurs in the articular extrem- 
ity of a bone the granulating medulla may send little offshoots through 
the articular cartilage. These may become fused together and inflam- 



668 



THE BOXES AND JOINTS. 



mation of the joint may follow. The walls of the shafts of the long 
bones may be converted into spongy tissue. If, as is sometimes the case, 
an ossifying periostitis occurs at the same time, the bone is thickened but 
spongy ; or sometimes there are concentric layers of compact bone tissue, 
separated by rarefied bone. 

Condensing Osteitis (Osteo-Sclerosis). — This lesion is characterized by 
the new formation of bone in the walls of the marrow cavities or Haver- 
sian canals. The bone is formed under the influence of the blood-vessels 
and osteoblasts, as in normal bone formation, but with less regularity. 
It may result in the conversion of cancellous tissue into compact bone, 
in the filling -up of the medullary cavity of long bones with more or less 
dense bone tissue. The compact bone, owing to the filling of its Haver- 
sian canals, may become very dense and ivory -like. When the medullary 




Fig. 397.— Condensing Osteitis, or Osteo-sclerosis, in Ulna of Child. 

a, Fragment of old bone with roughened, sinuous edges ; b, old Howship's lacunae covered with more re- 
cently formed bone lamellae ; c, d, new Haversian canals. 



cavities of long bones are involved the yellow marrow is converted into 
red marrow by the absorption of fat and increased vascularity. 

Osteo-sclerosis is frequently associated with ossifying periostitis. It 
often follows rarefying osteitis, and then the Howship's lacunae resulting 
from the original absorption process may be filled and covered in with 
new bone lamellae (Fig. 397). It is apt to occur in connection with 
necrosis or chronic inflammation of adjacent soft parts, but it sometimes 
occurs independently under unknown conditions. 

Suppurative Osteitis (Abscess of Bone). — This process occurs usually in 
the ends of the long bones, and is associated with rarefying osteitis. As 
the bone tissue is absorbed, a circumscribed cavity may be formed in the 
bone, filled with pus and lined with granulation tissue. 

Less frequently abscesses are formed in the shaft of a long bone by 
circumscribed suppuration of the medulla. Such abscesses may occur in 



THE BONES AXD JOINTS. 669 

old people and may be of long duration. They may gradually enlarge 
and be accompanied by an ossifying periostitis, so that the bone is ex- 
panded. The abscesses in suppurative osteitis sometimes develop rapidly 
and may perforate. On the other hand, instead of abscesses, there may 
be a diffuse infiltration with pus of the Haversian canals or of the spaces 
formed by rarefying osteitis (see Osteomyelitis, below). 

Osteomyelitis.-^— The tissues of the medulla so frequently share in the 
inflammatory processes in bone that many conditions described as osteitis 
are really osteomyelitis. It is custoinary, however, to reserve the latter 
name for those cases in which the medulla is primarily or chiefly involved. 

Acute Infectious Osteomyelitis.— This may occur as the result 
of a local injury which permits the access or favors the development of 
pyogenic micro-organisms ; it may be metastatic, resulting from the trans- 
portation of infectious material from other parts of the body in septi- 
caemia and i)yffimia, in typhoid fever, in the exanthematous fevers, and 
under other conditions ; or it may occur without evidence of local predis- 
position or of infectious processes in other parts of the body. 

The lesions of acute infectious osteomyelitis are, in the large majority 
of cases at least, due to the presence and action of the pyogenic cocci, 
the Staphylococcus pyogenes and the Streptococcus pyogenes, and in 
many of its forms it may be regarded as one of the phases of septicaemia 
or septico -pyaemia. 

While the lesions vary widely, the following general description is 
applicable to a considerable proportion of the cases : 

At the commencement of the disease, which usually begins in the shaft 
of one of the long bones, there are hyperaemia and oedema of the medulla, 
so that if the bone be opened the marrow is soft and of a dark-red color. 
A diffuse suppuration now rapidly ensues, and the marrow becomes 
streaked or mottled with gray. Occasionally, though not often, larger 
and smaller abscesses may form in the marrow. The inflammatory areas 
may be circumscribed ; or, in the more malignant cases, the entire mar- 
row may become rapidly involved. The cancellous tissue of one or both 
of the epiphyses usually becomes involved. The disease, however, is 
not commonly confined to the medullary spaces. The x)eriosteum becomes 
oedematous and infiltrated with pus, and the surrounding soft parts may 
become the seat of intense inflammatory changes. Abscesses of the peri- 
osteum or surrounding tissues are apt to form. As a result of these 
changes, necrosis of greater or less portions of the bone may ensue. The 
medullary cavity may become enlarged as pus accumulates, and the wall 
of the bone may be broken through, permitting the discharge of pus out- 
ward. Sometimes several bones are involved at once. Secondary in- 
volvement of the joints is very frequent. Here there may be only a 
serous or purulent exudation ; or the acute and destructive inflammatory 
process may extend beneath the joint and produce extensive alterations. 
In young persons the epiphyses verj^ frequently become separated from 
the shaft by the destruction of the cartilage which binds them together. 

In the severer cases, which are often called, par excellence, malignant 



670 THE BONES AND JOINTS. 

osteomyelitis, the changes may be very rapid and destructive. The 
medulla is disintegrated and gangrenous; the joints are soon involved; 
necrosis of large portions of the bone, sometimes of the whole shaft, 
occurs ; the periosteum and surrounding parts become gangrenous ; the 
veins contain thrombi , and pysemic infarctions and abscesses may form 
in various parts of the body. ^ 

Chronic Osteomyelitis. — In prolonged cases of osteomyelitis there 
is apt to be more or less ossifying periostitis and osteosclerosis, and 
fistulse may form in the bone, through which the exudates are dis- 
charged. ^ 

Tuberculous Osteitis is essentially a rarefying osteitis associated with 
the formation of tubercle tissue and cheesy degeneration. The tubercles 
are sometimes small, scattered, and miliary in form (see Fig. 398) ; some- 
times they unite to form larger and smaller masses. There may be 




V- 



Fig. 398.— Tuberculous Osteitis. 
A miliary tubercle formed in the cancellous tissue near the joint in tuberculous arthritis. 

extensive involvement of the medulla. There may be much simple gran- 
ulation tissue or the formation of abscess associated with the process. 
Condensing osteitis and necrosis are not infrequently present. Tuber- 
culous osteitis is often associated with tuberculous inflammation of the 
joints. It is most apt to occur in cancellous bone tissue, and is most 
common in the bodies of the vertebrae and in the carpal and tarsal bones. 
Syphilitic Osteitis. — Syphilitic infection may lead to one or other of the 
forms of osteitis just described, or gummatous nodules may form. Syph- 

^ Consult for an elaborate treatment of acute osteomyelitis in its relationship to other 
forms of inflammation, with bibliography, Jordan, Beitr. z. klin. Chir., Bd. x., p. 587. 
For a study of this condition in childhood see Koplik mid Van Arsdale, Am. Jour. Med. 
Sciences, vol. ciii., pp. 422 and 535, 1892. 

'^ For a resume of the deformities resulting from osteomyelitis consult Park, Medi- 
cal Record, November 2d, 1895. 



THE BONES AND JOINTS. 671 

ilitic osteitis usually commences in the periosteum, which becomes thick- 
ened and infiltrated with cells, so that there may be a circumscribed 
thickening of the periosteum, with or without distinct gummata. The 
vessels which extend from the periosteum into the bone become sur- 
rounded by new cellular tissue, which causes an enlargement of the 
canals. At this stage, if the periosteum be stripj)ed off, it drags with it 
the vessels surrounded by the new cell growth, leaving the bones beneath 
with numerous small perforations extending inward. As the disease 
progresses the channels in the bone enlarge by a rarefying osteitis and 
coalesce, forming large, irregular defects filled with new fibrous tissue. 
In these masses of new tissue, cheesy degeneration may occur, so that the 
new growth has more or less of the character of a gumma. In the vicin- 
ity of these gumma-filled spaces a condensing osteitis may occur, both in 
the substance of the bone and on the surface, in the form of osteophytes, 
so that the opening in the bone may be surrounded by an elevated, irreg- 
ular ring of bone tissue. All this may occur beneath the uninvolved 
skin, or the skin may participate by a suppurative inflammation, result- 
ing in ulcei^ation. These processes may be circumscribed or involve a 
large part of a bone. It is not infrequently associated with necrosis of 
larger and smaller portions of bone. The syphilitic tissue may be ab- 
sorbed and its place be more or less filled with fibrous tissue. Syphilitic 
osteitis is most frequent in the cranial bones, but may occur elsewhere, 
as in the sternum, clavicle, tibia and fibula, the ribs, etc. 

Congenital SypJiiUs. — The bones of young children in this condition 
may show increased density or evidences of periostitis, or irregular thick- 
enings, particularly of the skull. Characteristic lesions are frequently 
found in the long bones in still-born or young children who are the vic- 
tims of hereditary syphilis. These lesions are found for the most part 
along the border zone between the epiphysis and diaphysis. In normal 
ossification of the long bones, the border line between the calcification 
and ossification zones is narrow, sharply defined, and straight, or lightly 
and evenly curved. In the syphilitic bones, on the contrary, this line is 
broader, uneven, and presents various modifications, which merge into 
one another, so that all intermediate forms may be seen. In a lesion of 
moderate grade there may be, between the cartilage and the new -formed 
spongy bone, a white or reddish-white zone, about 2 mm. in breadth, 
with very irregular borders, consisting of calcified cartilage, in which the 
linear groups of cartilage cells are more abundant than normal. In more 
pronounced lesions the calcified zone, still containing an unusual number 
of cartilage cells, is broader and still more irregular and less sharply out- 
lined against the ossification zone. The cartilage just beyond it is softer 
and almost gelatinous, and may contain numerous blood-vessels, islets of 
connective tissue or of calcification, or irregular ossification. Finally 
the bone may be pouched out at the sides around the ossification and 
calcification zones, and the perichondrium and periosteum thickened. 
The whitish, irregular calcified zone is hard and friable. Between this 
and the new-formed bone there is an irregular, soft, gray or grayish- 



672 THE BONES AND JOINTS. 

yellow zone, from 2 to 4 mm. in thickness, which forms a loose, readily 
separated connection between the cartilage and the diaphysis. The 
white, friable zone consists mainly of irregular rows of degenerated aud 
distorted cartilage cells lying in a calcified basement substance, of irreg- 
ular masses of atypical bone tissue, and of blood-vessels surrounded by 
variously shaped cells. The soft zone consists of more or less vascular 
tissue with homogeneous basement susbtance, and round and spindle 
shaped cells. This soft zone is not sharply outlined against the adjoin- 
ing new-formed spongy bone, which, instead of consisting of the normal 
marrow spaces with bony lamellae beween them, is largely composed of 
granulation tissue. 

Different phases of this faulty development may be seen in different 
bones in the same individual. According to Wegner the lesion is usually 
most advanced in the lower end of the femur, then in the lower ends of 
the leg bones and of the forearm, then in the upper ends of the tibia, 
femur, and fibula. 

Not infrequently there is fatty degeneration of the marrow cells and 
blood-vessels, giving the marrow a reddish-yellow color. These altera- 
tions of the bones may occur, not only in children who have gummata in 
other parts of the body, but also in those in whom other evidences of 
syphilitic infection are absent. So uniform is their occurrence that their 
presence alone suffices for the establishment of a diagnosis. 

NECROSIS. 

Necrosis is the death of a larger or smaller portion of bone. This 
may be induced by conditions which deprive the bone of its proper vas- 
cular supply from the periosteum and medulla. It may be associated 
with suppurative periostitis, osteomyelitis, and osteitis, traumatic sepa- 
ration of the periosteum, ulcers of neighboring soft parts, emboli, the 
action of phosphorus vapor, and exhaustive infectious diseases. Necrosis 
is a pure form of gangrene, differing from gangrene of soft parts in that 
the dead bone has at first, and may retain for a long time, the general 
outward characters of the normal bone ; while in dead soft parts rapid ab- 
sorption may occur, or should bacteria of various forms be present, or gain 
access to the dead tissue, putrefaction, with conij)lex changes, may ensue. 

When a portion of bone has died inflammation occurs at the dividing- 
line between the dead and living bone. This inflammation has the char- 
acters of a rarefying osteitis (see above), and finally separates the dead 
from the living bone. The dead bone, or sequestrum, may remain smooth 
and unaltered (Fig. 399), or it may be eroded by the influence of sur- 
rounding pus or granulation tissue or osteoclasts. In this way it is pos- 
sible for the sequestrum, if it be small, to be entirely absorbed. More 
frequently there is a production of new bone around the sequestrum, 
either beneath the periosteum or in the substance of the bone, and this 
becomes lined with granulation tissue, from which pus may continue to 
be formed, bathing the sequestrum. 



THE BONES AND JOINTS. 673 

Necrosis may involve the superficial layers, or the entire thickness of 
the wall of a long bone, or only the spongy tissue and inner layers, or an 
entire bone, or a number of different portions of the same bone, but it is 
most apt to occur in comi)act bone. 

The death and separation of the bone may be soon followed by the 
growth of new bone to repair the loss. The periosteum, the medulla, 
and the surrounding soft tissues may all take part in this new growth. 
The new bone is usually irregular, rough, and perforated with openings 
through which pus formed around the sequestrum may be discharged. 
If the sequestrum be removed, healing may occur by the formation of new 
bone ; but the bone is usually more or less distorted by the irregular new 
ossification. 

FJwsphoriis Necrosis. — Under the influence of phosphorus vapor, peri- 
ostitis and osteitis, particularly of the jaw, are apt to occur, which 




Fig. 399.— Necrosis of bone. 

Showing sequestrum of dead bone partially surrounded by new-formed subperiosteal bone, with thickening 

of the shaft. 

usually lead to more or less extensive necrosis, generally associated with 
prolonged and often extensive suppuration. 

CARIES. 

Caries of bone is essentially an ulcerative osteitis resulting in progres- 
sive molecular destruction of the bone tissue. It differs from necrosis in 
that, in the latter, larger and smaller masses of bone die, while in caries 
the destruction is molecular and gradual. It may occur in connection 
with any form of osteitis, with periostitis and osteomj^elitis, or it may be 
secondary to inflammatory or destructive processes in the joints or adja- 
cent soft parts. The depressed surfaces of bones in which caries is pro- 
gressing are rough and more or less finely jagged, and may be covered 
with granulations. The minute changes by which ulceration and destruc- 
tion of the bone are produced in caries are somewhat analogous Avith those 
ill rarefying osteitis, but there are marked degenerative changes in the 
bone cells, which may become fatty or converted into a granular ma- 
terial. Moreover, the basement substance of the bone, instead of being 
absorbed, may disintegrate, with the formation of larger and smaller 
masses of detritus. Sometimes the lime salts are removed from the base- 
43 



674 THE BONES AND JOINTS. 

ment substance, which is converted into atypical fibrillar tissue and fatty 
and granular detritus. Very extensive suppurations and necrosis may 
be associated with caries. 

Long-continued caries, especially in badly nourished individuals, is 
apt to become complicated with tuberculous inflammation. 

There is very little tendency to spontaneous healing in caries, but it 
may occur, and the defects produced may be more or less supplied by 
means of new-formed bone. 



RACHITIS. (Rickets.) 

Eickets is a developmental disease of bone, in which the proper ossi- 
fication does not take place. The disease usually occurs during the first 
two years of life, but may be congenital, ' or may occur as late as the 
twelfth year. 

The physiological growth of bones presents three phases. They grow 
in length by the production of bone in the cartilage between the epiphy- 
sis and diaphysis ; in thickness, by the growth of bone from the inner 
layers of the periosteum. At the same time the medullary canal is en- 
larged, in proportion to the growth of the bone, by the disappearance of 
the inner layers of bone. 

In rickets these three phases of growth are abnormal. The carti- 
laginous and subperiosteal cell growth, which precedes ossification, goes 
on with increased rapidity and exuberance and in an irregular manner, 
both between the epiphyses and diaphyses and beneath the periosteum, 
while the actual ossification is imperfect, irregular, or wanting. At the 
same time the dilatation of the medullary cavity goes on irregularly 
and often to an excessive degree. 

If one examine microscopically in a rachitic bone the region between 
the epiphysis and diaphysis (Fig. 400), he finds that the cartilage cells 
are not regularly arranged in rows along a definite zone in advance of the 
line of ossification, as in normal development, but that there is an irreg- 
ular heaping-up of cartilage cells, sometimes in rows, sometimes not, 
over an ill -defined and irregular area. The zone of calcification also, 
instead of being narrow, regular, and sharply defined, is lacking in uni- 
formity. Areas of calcification may be isolated in the region of prolifer- 
ating cartilage cells, or calcification may be altogether absent over con- 
siderable areas. 

Corresi^onding to these irregularities the ossification zone is also irreg- 
ular. New-formed bone and marrow cavities containing blood-vessels 
may lie in the midst of the cartilage, or masses of cartilage may lie deep 
in the region which should be completely ossified. In other places it 
seems as if the cartilage tissue were directly converted into an ill-formed 
bone tissue by metaplasia or direct transformation. It will readily be 
seen from this that the medullary spaces of the new -formed bone are 

' Salvetti, Ziegler's Beitrage z. path. Anat., etc., Bd. xvi., p. 29, 1894, bibliography. 



THE BOXES AXD JOIXTS. 



675 



irregular, and this abnormality is enhanced by the premature intra-med- 
uUary absorption of the bone. 

Similar irregularity in the bone formation may be seen beneath the 
periosteum. An excessive proliferation of cells in the inner layers of 
the periosteum, the irregular calcification which occurs about them, and 
the absence of uniformity in the elaboration of ill -structured bone, con- 
spire to produce an irregular, spongy bone tissue instead of the compact, 
lamellated tissue which is so necessary here for the solidity of the struc- 
ture. The increased cell growth between the epiphj'ses and cliaphyses 
produces the peculiar knobby swellings which are characteristic of rickets. 
At the same time the medullary cavity increases rapidly in size and the 
inner layers of the bone become spongy. The medulla may be congested, 











Fig. 400.— Rachitic Bo.ne. 
Showing ossiflcation zone in a longitudinal section of a rib. 



and fat, if it has formed, may be absorbed, and a modified form of 
osteitis may ensue. 

The result of these processes is that the bones do not possess solidity 
and cannot resist the traction of the muscles or outside pressure. The 
epiphyses may be displaced or bent, especially in the ribs, less frequently 
in the long bones. The long bones and the pelvic bones may be bent 
into a A^ariety of forms. Incomplete fractures are not infrequent. Com- 
plete fractures do not usually occur until the later stages of the disease, 
when the bones have become more solid. In the head, the cranium may 
be unnaturally large for the size of the face ; the f ontanelles and sutures 
may remain open ; the bones may be soft, porous, and hyiiersemic, while 
at their edges there may be rough, bony projections beneath the pericra- 
nium. Sometimes, especially in the occipital bone, there are rounded 
defects in the bone, filled only with a fibrous membrane ; this constitutes 
one of the forms of so-called Craniotabes (Fig. 401). 



676 



THE BONES AND JOINTS. 



It does not fall within the scope of this work to describe the various 
deformities which may occur as a result of this disease. The familiar 
pigeon breast ; the rows of knobs along the sides of the chest from bend- 
ing and dilatation of the ribs at the point of junction of cartilage and 
bone ; the knock-knees, bow-legs, spinal curvatures, etc. , may all be the 
result of rachitic weakening of the bones. 

After a time the rachitic process may stop and the bones take on a 
more normal character. The porous bone tissue becomes compact and 
even unnaturally dense ; the swellings at the epiphyses disappear ; many 
of the deformed bones may become of a normal shape. In severe cases, 
however, the deformities continue through life ; especially is there a ces- 




Fig. 401.— Craniotabes. 

This skull of a child is large, its bones are thin, with holes due to faulty development and covered only by 

a thin, fibrous membrane. 



sation of the growth of the bones in their long axis, so that the persons 
affected are dwarfed. 

The disease may have an acute or a chronic character. The acute 
form begins usually during the first six months of life. The children are 
apt to suffer from vomiting, diarrhoea, profuse sweating, chronic bron- 
chitis and pneumonia, general ansemia, and wasting. They either die or 
the rachitic process is gradually developed. The chronic form is seen in 
older children, and often in those apparently healthy. The changes in 
the bones may take place without constitutional symptoms, though there 
are often catarrhal bronchitis, pneumonia, and anaemia. 



THE BONES AND JOINTS. 677 



OSTEOMALACIA. 

This lesion consists in the softening of fully formed hard bone tissue 
by the removal of its inorganic salts. It is to be distinguished from 
rickets, whose lesions are due to a faulty development of bone, although 
in certain external characters the two diseases sometimes present consid- 
erable similarity. Osteomalacia usually occurs in adults, most fre- 
quently in females during pregnancy and after parturition ; more rarely 
it occurs in males, and in females unassociated with the above conditions. 
Its cause is not known. 

Microscopical examination shows that the decalcification occurs first in 
the periphery of the Haversian canals and in the inner layers of the walls 
of the marrow spaces. As the salts of lime are removed the basement 
substance at first remains as a finely fibrillated material, still preserving 
the original lamellation. The bone cells may be changed in shape or 
degenerated. After a time the decalcified tissue may disintegrate and 
be absorbed, and its iDlace occupied by new-formed marrow or granula- 
tion tissue. As the disease goes on the marrow tissue is congested and 
red, the fat absorbed, and there is a great accumulation of small sphe- 
roidal cells ; or the marrow may assume a gelatinous appearance. The 
decalcification and absorption of the bone from within may proceed so 
far that the bony substance in the cancellous tissue almost entirely dis- 
appears, and the compact bone is reduced to a thin, soft, decalcified tis- 
sue. The disease is not always continuously progressive, but may be 
subject to temporary cessation. 

As a result of this softened condition of the bones, the weight of the 
body and the actions of the muscles may induce a series of deformities 
which are sometimes excessive ; curvatures of the spine, complete and 
incomplete fractures of the bone, distortions of the pelvis, sternum, etc. 
There is a tendency in this disease to a general involvement of the bones, 
but the changes are sometimes confined to single bones or groups of 
bones. The cranium is rarely much affected. 



ALTERATIONS OF THE BONE MARROW IN LEUKAEMIA AND 

ANiEMIA. 

In certain forms of leuksemia the marrow of the bones is very 
markedly altered. The change consists mainly in an accumulation in 
the marrow tissue of spheroidal cells, often in a condition of fatty degen- 
eration, which lie in the meshes of reticular connective tissue and in and 
along the walls of the blood-vessels. There may also be absorption of 
the fat, and sometimes enlargement of the marrow cavity from absorp- 
tion of the bone. These alterations seem to be primarily due to an 
hyperplasia of the marrow cells. The new cells which accumulate in the 
marrow under these conditions are of various forms. Most characteristic 
are colorless, spheroidal cells which considerably resemble the large 



678 THE BONES AND JOINTS. 

lympliocytes of normal blood (see page 346 ) . But they are usually larger, 
though varying much in size, have one large, often vesicular nucleus 
staining less strongly than the lymphocyte nuclei, while the protoplasm 
usually contains neutrophile granules. These cells are called myelocytes 
(page 350). In addition to these the marrow may contain, mingled with 
its usual elements, nucleated red blood cells, spheroidal cells containing 
red blood cells, and not infrequently considerable numbers of small 
octahedral crystals (called Charcot's crystals). 

The degree to which this accumulation of cells occurs varies much in 
different cases, and the gross appearances of the marrow are consequently 
very diverse. In some cases the marrow is soft and has a uniform red 
appearance, or it is variously mottled with gray and red. Occasionally 
circumscribed haemorrhages are seen. In another class of cases, in which 
the cell accumulation is more excessive, the marrow may be gray, 
grayish-yellow, or puriform in appearance. 

These changes may occur in the central marrow cavity, as well as in 
the marrow spaces of the spongy bone. They may be present in several 
or many of the bones. They are usually accompanied by analogous 
changes in the spleen and lymph-nodes. 

In certain cases of acute and chronic anwmia, particularly in the perni- 
cious and progressive varieties, the marrow, especially of the larger long 
bones, may lose its yellow color from absorption of the fat, and become 
red. Microscopical examination of the marrow under these conditions 
may show myelocytes and sometimes an abundance of developing nucle- 
ated red blood cells and Charcot's crystals. 

In many of the acute infectious diseases, typhus and typhoid fever, 
ulcerative endocarditis, recurrent fever, etc. , the bone marrow has been 
found hypergemic, and may, it is asserted by Ehrlich, contain myelocytes 
in increased numbers. 

All these lesions of the marrow, although our knowledge of them 
is still very incomplete, together with what is known of the physiological 
functions of the marrow, point to a close relationship between the mar- 
row and the spleen and lymph-nodes as blood-producing organs. 



TUMORS. 

Tumors of the bone may involve either the periosteum, or the com- 
pact bone, or the medulla ; or, as is more frequently the case, two or 
more of these structures may be involved at once. Tumors of the bone 
are usually accompanied by various secondary and sometimes very marked 
alterations of the bone tissue, osteo-porosis, osteo-sclerosis, ossifying peri- 
ostitis, etc. The new growths are very apt to undergo calcification and 
ossification. 

Fibromata may grow from either the periosteum or the medulla. 
Their most common seat is in the periosteum of the bones of the head and 
face. They are apt to form polypoid tumors projecting into the posterior 
nares, pharynx, mouth, and antrum of Highmore. Central fibromata, 



THE BONES AND JOINTS. 679 

i.e., those growing from the medulla, are rare. They usuallj^ occur in 
the lower jaw^ but have been found in the ends of the long bones, the 
phalanges of the fingers, and the vertebrae. The fibromata may calcify 
or ossify, contain cysts, and not infrequently occur in combination with 
sarcoma. 

Myxomata are of occasional occurrence in bone. 

Osteomata. — Xew formations of bone as a result of inflammatory proc- 
esses are, as we have already seen, of frequent occurrence in bone, and 
although not, strictly speaking, tumors, some of their forms are very 
closely allied to them, and they may therefore be conveniently mentioned 
liere. ^NTew growths of bone which arise from the surfaces are called 
exostoses (see Fig. 395) or enostoses, according to their origin from the 
external surface or from the interior of the bone. They may contain all 
the constituents of normal bone : bone, medulla, vessels, periosteum, and 
cartilage. The new bone may be compact and like ivory, or spongy, or 
contain large cavities filled with marrow. 

The shape of exostoses varies greatly ; they may be in the form of 
sharp, narrow si)icula and processes, and, occurring in connection with 
periostitis, are called osteojyJiytes. They may be polypoid in shape, or 
form rounded tumors with a broad base. They may form a general 
enlargement of the bone with much roughening of the surface ; this con- 
dition is often called hyperostosis. 

The bone beneath these new growths may be normal, or sclerosed, or 
rarefied, or the medullary cavity of the bone may communicate with that 
of the exostosis. Exostoses are usually developed from the periosteum, 
sometimes in the insertion of tendons and ligaments. They are veiy 
frequently multiple, and may occur at all ages, even during uterine life. 

Enostoses are developed in the interior of bones from the medulla. 
They may increase in size, with absorption of the surrounding bone, until 
they project from the surface like exostoses. Their most frequent situa- 
tion is in the bones of the cranium and face. 

Chondromata. — These tumors may be single or multiple, and most fre- 
quently grow from the interior of the bone, but sometimes from the 
periosteum. They are prone to form various combinations with other 
forms of tumors, as fiboma, myxoma, sarcoma, etc. They are frequently 
congenital, and are most common in young people. They occur most 
frequently in the bones of the hand and foot. 

There is a form of chondroma, called osteoid chondroma, which develops 
beneath the periosteum, most frequently in the femur and tibia near the 
knee joint, forming a club-shaped enlargement of the bone. The char- 
acteristic of the tissue composing these tumors is that it resembles some- 
what the immature bone tissue which is seen beneath the periosteum 
in developing bone. It differs from cartilage in the irregular shape of 
its cells, in the fibrillation and density of the basement substance, and in 
its general vascularity. On the other hand, it has not the inorganic con- 
tents or appearance of true bone. It resembles considerably the callous 
tissue forming about fractures of the bones. It may, however, and most 



680 THE BOXES AND JOINTS. 

frequently does, become converted, in some parts of the tumor, into true 
bone. On the other hand, combinations with sarcomatous tissue are of 
frequent occurrence (see below). 

Sarcoma is especially common in the bones. It grows from the inner 
layers of the periosteum or from the medulla, so that we may distinguish 
a periosteal and a myelogenic sarcoma. Sometimes the tumor involves the 
bone itself so early that it is impossible to say whether the tumor l)egan 
in the periosteum or in the medulla. There is also a variety which grows 
close to the outside of the periosteum and becomes connected with it — 
parostecd sarcoma. 

The periosteal sarcomata usually belong to the varieties fibro-, myxo-, 
chondro-, and osteo -sarcoma, more rarely to the medullary variety. 
They commence in the inner layers of the ]Deriosteum, pushing this mem- 
brane outward. After a time the periosteum is involved and the tumor 




Fig. 403.— Sarcoma of the Bone— Periosteal. 

The growth has invaded the shaft of the bone, which is fractured. Spicula of bone, new formed in the 
tumor, may be seen below, passing outward from the periosteum, 

invades the surrounding soft parts. The bone beneath may remain nor- 
mal, or may be eroded and gradually disappear until the tumor is con- 
tinuous with the medulla. Portions of the tumor may be calcified, or a 
growth of new bone may accompany its growth. The new bone usually 
takes the form of plates, or spicula, radiating outward (Fig. 402). The 
minute structure of these tumors is very variable. The simplest — the 
fibro -sarcomata — are composed of fusiform, round, stellate, and some- 
times giant cells (myeloplaxes), in varying proportions, packed closely 
in a fibrous stroma. In the medullary form the stroma is diminished 
to a minimum and the round cells are most numerons. In the chondro- 
and myxo -sarcoma the basement substance may be hyaline or mucous, 
and the cells follow the type of cartilage and mucous tissue more or less 
closely. There is a mixed form of tumor, called osteoid sarcoma, which 
is very apt to spread and to form metastases. The growth consists in 
part of tissue corresponding to fibro-sarcoma and round-celled sarcoma. 
In addition to this there occurs, in greater or less quantity, immature 



THE BONES AND JOINTS. 681 

bone tissue, called osteoid tissue, which may in part become calcified, the 
calcification usually occurring in the central j)ortions, leaving a softer 
peripheral zone. This form of tumor is most apt to occur at the ends of 
the long bones, and may form tumors of large size. It is often called, 
on account of its tendency to extend and to form metastases, maUgnant 
osteoma or osteoid cancer. Angio- sarcomata are of frequent occurrence in 
bone. 

Sarcomata may originate in the medulla — myelogenic' — and may grow 
rapidly. The bone surrounding them is destroyed and they j)roject as 
rounded tumors. Most frequently new bone is formed beneath the peri- 
osteum, so that the tumor is enclosed in a thin, bony shell; sometimes 
there are also plates of bone in the tumor ; sometimes the periosteum is 
unaltered ; sometimes it is perforated and the tumor invades the sur- 
rounding soft parts. The tumors are frequently very soft, vascular, and 
hsemorrhagic in parts, or may enclose cysts filled with tumor detritus 
and blood. They are usually of the spindle or round celled variety, and 
not infrequently contain giant cells. 

Sarcomata may originate in the outer layers of the periosteum 
^parosteal. They may be as firmly connected with the bone as is 
the periosteal form. The periosteum may remain intact between the 
tumor and the bone, or it may disappear and leave them in apposition. 
Endothelioma of bone is not uncommon. 

Angioma, — A very large number of the tumors which have been 
described under this name are really very vascular sarcomata. Caver- 
nous angiomata may form between the periosteum and bone and inti- 
mately connected with the latter. There are several cases described of 
cavities filled with blood in the interior of bones, which it is difficult to 
interpret. They have mostly been found in the head of the tibia. They 
are said to have consisted of single sacs comjDOsed of thickened 
periosteum, lined with plates of bone, and filled with fluid and clotted 
blood. ]^o large vessels communicated with the sacs, but their walls 
were covered with a rich vascular plexus, branches of which opened into 
the cavity of the sac. 

Carcinoma. — Primary carcinoma is of doubtful occurrence in the 
bones. Most of the structures thus named have doubtless been sar- 
comata or endotheliomata. Secondary carcinoma, on the other hand, 
as a result of metastases or local extension, is not infrequent. Metas- 
tatic carcinomata may occur in the bones of various parts of the body 
at the same time, and are most apt to be secondary to carcinoma of the 
mamma. 

Cysts. — These most frequently occur in the maxillary bones, doubtless 
in connection with the teeth. They may be unilocular or multilocular, 
and contain clear serum or a mucous or brown fluid, and sometimes cho 
lesterin. They may be lined with epithelium. They begin in the interior 
of the bone, and, as they increase in size, expand it until they may be 

iSee Wright, "Multiple Mj-eloma," Trans. Assn. Am. Plij'S., vol. xv., p. 137, 1900; 
also Winkler, Yirchow's Arch., Bd. clxi., pp. 252, 508, 1900. 



682 THE BONES AND JOINTS. 

covered with ouly a thin shell of bone. They may reach a large size, 
even as large as a child's head. 

Dermoid Cysts are occasionally found in connection with the bones, 
particularly of the skull. ' 

The Joints. 

For a description of the dislocations, misplacements, and injuries of 
the joints we refer to works on surgery. 



DEGENERATION. 

Fatty degeneration of the cartilage cells, mucous degeneration, and 
fibrillation of the stroma with softening, and often roughening, of the 
joint surfaces, calcification and amyloid degeneration, may occur in 
inflammation, or as a senile alteration, or under other conditions. The 
cartilage is usually, under these conditions, whiter and more opaque than 
normal. 

INFLAMMATION. (Arthritis.) 

Exudative Arthritis, — The earlier stages of acute inflammation of the 
synovial membranes are better known from experiments on animals than 
from post-mortem examinations. The first changes are swelling and 
congestion of the membrane, with increased growth and desquamation of 
the lining cells, and infiltration of the membrane with lymphoid cells. 
These conditions are soon followed by an exudation. 

In Serous Arthritis the accumulation of serum within the synovial sac 
is the most iDrominent lesion. The disease may terminate in recovery, or 
become chronic, or pass into the suppurative form. It may be incited 
by contusions, penetrating wounds, gonorrhoea, rheumatism, or it may 
occur without evident cause. 

Sero-fibrinous Arthritis may occur under the same conditions as those 
which lead to simple serous inflammation. The fibrin may be present 
largely as flocculi in the serum, or it may form false membranes over the 
surfaces of the joint. 

Suppurative Arthritis may follow or be associated with the above forms 
of inflammation. The synovial membrane is thickened and cloudy, and 
there may be but a moderate amount of pus in the joint, and a slight 
degree of infiltration of the synovial membrane with pus cells. Under 
these conditions resolution may occur. 

In other cases the accumulation of pus in the cavity may be great, 

the synovial membrane and its surrounding tissue densely infiltrated 

with pus cells. Under these conditions granulation tissue is apt to 

form and the cartilages of the joints are apt to become involved. 

There are swelling and proliferation or degeneration of the cartilage 

^ For a resume and bibliography of the pathology of bone see Schmidt in Lubarsdi 
and Ostertag's ''Ergebnisse," Jahrg. iv. for 1897, p. 531; also Jahrg. v. for 1898, p. 895. 



THE BONES AND JOINTS. 683 

cells; the basement substance becomes disintegrated, ulcerates, and 
exposes the bone, in which osteitis, caries, rarefaction, etc. , may occur. 
The new-formed granulation tissue may penetrate the cartilage, absorb- 
ing the basement substance, and by metaplasia the cartilage tissue may be 
converted into embryonal or granulation tissue. The pus may break 
through the capsule of the joint and form large abscesses in the adjacent 
soft parts. Sometimes the inflammation is not only suppurative but gan- 
grenous, and runs a rapidly fatal course. The synovial membrane, artic- 
ular cartilages, and ends of the bone all undergo a rapid suppuration 
and gangrene. Acute arthritis may be incited by trauma, or it may 
be associated with pyaemia, smallpox, measles, scarlet fever, pneumonia, ' 
gonorrhoea," diphtheria, mumps, typhus fever, glanders, the puerperal 
condition, or other infectious diseases. In these cases the process is apt 
to be suppurative, and is induced by various forms of bacteria. 

Chronic Arthritis may begin as such, or it may be the result of previous 
acute inflammation. There is an increase of fluid in the joint. This 
fluid is thin and serous, or is thickened with flocculi of fibrin and epi- 
thelial and lymphoid cells, or is thick, syrupy, or even gelatinous. The 
synovial membrane is at first congested, its tufts are prominent. Later it 
becomes thickened, sclerosed, and anaemic ; the epithelium is destroyed, 
and the tufts become large and projecting. From the distention of the 
capsule there may be subluxations or luxuations of the joint, or the cap- 
sule may be ruptured. 

Rheumatic Arthritis. — An acute inflammation, usually exudative in 
character and involving one joint after another, is characteristic of acute 
articular rheumatism. The exudate is usually serous. 

A chronic form of so-called rheumatic arthritis is most common in 
elderly persons, usually affecting several joints and advancing slowly and 
steadily. There is a fibrous thickening of the synovial membrane and 
the adjacent tissue. Fluid accumulations are not common. The artic- 
ular cartilages are apt to degenerate or ossify, or become softened and 
fibrillated, and they may disappear. The contracting synovial mem- 
branes and fibrous tissue render the joints stiff and may cause consider- 
able deformity. Not infrequently fibrous and bony ankyloses are formed 
between the ends of the bones. 

Arthritis deformans. — This name has been applied to a variety of 
chronic inflammation of the joints which, combined with degeneration of 
parts of the joint and the new formation of bone, may result in marked 
deformities of the part. 

It usually occurs in elderly persons and is apt to involve several 
joints, most frequently the hip, knee, fingers, and feet. It may be idio- 
pathic, or due to rheumatism or to injuries, or follow an acute arthritis. 
The capsules of the affected joints are thickened and sclerosed. The 
synovial fluid is at first increased in quantity ; later, diminished and 
thickened. The tufts of the synovial membrane become much enlarged 

Tor bibliography of pneumococcic arthritis, see Cave, Lancet, 1901, vol. i., p. 82. 
'^ See bibliography, p. 194. 



684 THE BONES AXD JOINTS. 

and vascular ; they may be converted into cartilage. Sometimes the cap- 
sule becomes ossified. The new bone grows from the edge of the carti- 
lage within the capsule and its articular surface is covered with cartilage. 
The articular cartilages are much changed. The basement substance 
splits into tufts, while the cartilage cells are increased in number. Or 
the basement substance becomes fibrous ; or it is split into lamellae and 
the cartilage cells are multiplied ; or there are fatty degeneration and 
atrophy. 

As a result of these changes, larger or smaller portions of the cartilage 
are destroyed and the bone beneath is laid bare. The exposed bone may 
become compact and of an ivory smoothness. The ends of the bones are 
much deformed. They are flattened and made broader hj irregular new 
growths of bone, while at the same time they atrophy. The new growth 
of bone starts from the articular cartilages. The cartilage cells increase 
in number and the basement substance grows in quantity. This growth 
is most excessive at the edge of the cartilage, so that a projecting rim is 
formed there. This projecting rim may ossify next the bone, and at the 
same time new cartilage may form on its surface, so that we may find 
large masses of bone covered with cartilage. All these changes occur in 
various combinations and sequences, so that joints in this condition pre- 
sent the greatest variety of appearances. 

Arthritis TJritica (Gouty Arthritis). — This lesion is characterized by the 
deposit of salts of uric acid in the cartilages, bones, and ligaments, and 
also in the cavities of joints. The deposits may be in the form of stellate 
masses of acicular crsytals in and about the cartilage cells or in the base- 
ment substance ; or they may be deposited in the fibrillar connective- 
tissue structures of the joint in single crystals, or in the subcutaneous 
tissue about the joint as white concretions. The deposits may occur in 
repeated attacks of the disease, and are accompanied by acute inflam- 
matory changes. They may lead to various forms of chronic inflamma- 
tion of the joints. 

Tuberculous Arthritis. — This process may commence in the joint itself, 
or may extend to it from adjacent bone. It is characterized by the for- 
mation of tubercle tissue and granulation tissue, sometimes in great quan- 
tity, and is usually associated with secondary inflammatory and degener- 
ative changes of surrounding parts. According to the prominence of 
one or other of these secondary alterations, several forms of tuberculous 
arthritis may be distinguished. If there is an excessive growth of gran- 
ulation tissue without much suppuration, this constitutes a ftingous form. 
Sometimes there is extensive siqypiDXition, so that the cavity of the joint 
may be filled with pus, which may be discharged through openings in 
the skin ; or there may be more or less extensive formation of abscesses, 
or infiltration of the soft parts about the joint with pus. In other cases 
there is disintegration of the new-formed tuberculous tissue and of the 
tissues of the joint — ulcerative form. The cartilage basement substance 
may become split into fragments and the cells degenerate, and thus deep 
and destructive ulcers of the cartilage may be formed. Or the new tissue 



THE BONES AND JOINTS. 685 

may work its way through the cartilage into the bone beneath, by absorp- 
tion of the basement substance of the cartilage, with or without prolifer- 
ation of its cells. Caries and necrosis of the underlying bone may lead 
to extensive destruction. Hand-in-hand with these alterations subperi- 
osteal new formation of bone may occur, or sclerosis of the adjacent 
bone tissue. There may also be a great increase of fibrous tissue about 
the joint. 

This disease is most common in children and young persons. The 
so-called scrofulous diathesis is said to foster it, but local injuries are 
frequently the predisi)Osing factors. It is most common in the large 
joints. It may occur in connection with tuberculous inflammation in other 
parts of the body, but it is frequently quite local, and may remain so 
for a very long time or permanently, since general infection from tuber- 
culous arthritis is comparatively infrequent. 

The process is usually slow, and may end in death. If recovery takes 
place before the cartilages and bones are involved, the joint is preserved; 
but it may be stiffened, or even immovable, from the contraction of the 
new fibrous tissue around it. If the cartilages and bones are diseased 
the joint is destroyed, and either bony or fibrous ankylosis results. 
Sometimes, from the change in the articulating surfaces and the contrac- 
tion of the muscles and the new fibrous tissue, partial or complete dis- 
locations are produced. 

Occasionally miliary tubercles occur in the synovial membranes in 
cases of general miliary tuberculosis, with but little accompanying simple 
inflammatory change. 

TUMORS. 

Secondary tumors of the joints as a result of local extension from the 
adjacent parts are not uncommon, and the tumors may be of various 
kinds. Primary tumors of the joints, on the contrary, are not very 
common. 

Lipoma. — A new growth of fat tissue may begin in the other portions 
of the synovial membrane, push this inward, and project into the joint 
in a mass of tufts — lipoma arborescens. 

Fibroma occurs as an hypertrophy of the little tufts and fringes of the 
synovial membrane. In this way large polypoid and dendritic bodies 
are formed. The pedicles of these growths may atrophy and even dis- 
appear, so that the growths are left free in the cavities of the joints. 

Corpora aliena Articulorum (Loose Cartilages in the Joints). — This name 
is given to bodies, of various structure and origin, which are found free 
or attached by slender pedicles in the cavities of the joints. They are 
most frequently found in the knee ; next in order of frequency in the 
elbow, hip, ankle, shoulder, and maxillary joints. They may be single 
or in hundreds. Their size varies from that of a pin's head to that of 
the patella. They are polypoid, rounded, egg-shaped, or almond- 
shaped ; their surface is smooth or faceted, or rough and mulberry -like. 



686 THE BONES AND JOINTS. 

They are composed of fibrous tissue, cartilage, and bone in various pro- 
portions. 

These bodies are formed by hyperplasia of the synovial tufts and 
the production in them of cartilage and bone. 

More frequently the small plates of cartilage form on the inner surface 
of the synovial membrane, which increase in size while their outer layers 
ossify. These may remain fixed in the synovial membrane ; or they pro- 
ject and become detached from it, and they then appear as flattened, 
concave bodies composed of bone covered with cartilage on one side. 

On the other hand, cartilage and bone may form outside the synovial 
membrane from the periosteum or the edges of the articular cartilages, 
and pushing inward, may later become detached. 

Earely portions of the articular cartilages may be detached by vio- 
lence or disease ; or fibrinous and other concretions may form in arthri- 
tis, or under conditions which we do not understand. 



CHAPTER XIII. 

VOLUNTARY MUSCLE. 

NECROSIS. 

I^ECROSis of muscle may be the local result of mechanical or chemical 
injury ; it occurs in inflammatory foci, and may follow serious local dis- 
turbances of the circulation, as from pressure by tumors or cicatrices, etc. 
The muscle fibres may gradually lose their striations, become granular and 
disintegrate, or the muscle substance may become homogeneous and 
strongly refractile and break into irregular masses. I^ecrotic muscle 
fibres are finally removed by the direct action of phagocytes or after 
various transformations leading to solution. 



ATROPHY AND HYPERTROPHY. 

Simple Atrophy. — This may occur in old age, in prolonged exhausting 
diseases, or as a result of pressure from a foreign body, tumors, etc. 
The muscle fibres grow narrower, the degree of narrowing frequently 
varying considerably in different parts. They usually retain the stria- 
tions, but these may be obscured by degenerative changes. The sarco- 
lemma may become thickened, and there may be a considerable increase 
in connective tissue between the muscle fibres and bundles. Brown pig- 
ment particles may accumulate in the atrophied fibres. 

Progressive Muscular Atrophy. — This lesion consists essentially in a 
combination of simple or degenerative atrophy of the muscle fibres with 
chronic interstitial inflammation, and is sometimes associated with pro- 
liferative changes in the muscle nuclei. In the earlier stages of the dis- 
ease the muscles may be pale and soft, but exhibit otherwise to the naked 
eye but little alteration. Gradually, however, the muscle substance be- 
comes replaced by connective tissue, so that in marked and advanced 
cases the muscles are converted into fibrous bands or cords, whose cica- 
tricial contraction may induce great deformities. 

Microscopical examination shows in the early stages of the disease a 
proliferation of cells in the interstitial tissue, so that this may have the 
appearance of granulation or embryonal tissue ; also in some cases marked 
proliferative changes in the muscle nuclei (Fig. 403), leading to the 
formation of new cells which may more or less replace the contractile 
substance within the sarcolemma. The new interstitial tissue increases 
in quantity and grows denser, and may crowd the muscle fibres apart 



688 



VOLUNTARY MUSCLE. 



(Fig. 404). The walls of the blood vessels may also become thickened. 
Hand-in-hand with these interstitial alterations the atrophy of the muscle 
fibres proceeds. These may simply grow narrower, retaining their stria- 
tions; or they may split up into longitudinal fibrillse, or transversely 
into discoid masses, and in this condition disappear. In other cases a 
certain amount of fatty or hyaline degeneration may be present. These 
degenerative and proliferative changes do not, as a rule, occur uniformly 
in the affected muscles, but some parts are affected earlier and more 
markedly than others. The atrophied muscle may be replaced by fat. 

Progressive muscular atrophy is apt to commence in the small muscles 
of the extremities, in many cases in the muscles of the ball of the thumb. 
It may commence in the muscles of the shoulder, the arms, or the back. 



d. 



^"-_ 
'^^,® 



y^^'^^^^- 













Fig. 403 —Progressive Muscular Atrophy (Soleus muscle, longitudinal section). 

a, Atrophied muscle fibre ; ft, degenerated muscle fibre ; c, interstitial tissue ; d, clusters of proliferated 

muscle nuclei. 



It may have a continuous extension, or it may jump single muscles or 
groups of muscles. Death may be induced by the affection of the 
muscles of respiration or deglutition. 

The causes of this lesion are in many cases unknown, and there is 
considerable lack of unanimity of opinion as to whether it is primarily a 
disease of the muscles or of the nervous system. In a considerable pro- 
portion of cases the muscle lesion is associated with atrophy of the gan- 
glion cells in the anterior cornua of the spinal cord and the develojDmeut 
of connective tissue about them. In other cases these changes in the 
cord may apparently be absent. 

It is sometimes accompanied by atrophy of the nerves which are dis- 
tributed to the muscles, and atrophy of the anterior roots has been 
described. 

It is probable that there are several varieties of progressive muscular 
atrophy, which our present knowledge does not enable us clearly to dis- 
tinguish. Muscular atrophy in some cases follows overstraining of groups 



VOLUNTARY MUSCLE. 689 

of muscles, or injuries, and may occur as one of the sequelae of typhoid 
fever and diphtheria. 

Hypertrophy. — True hypertrophy of muscle as a pathological condition 
is rare, but it has been described in a few cases. It is usually confined 
to circumscribed groui^s of muscles. On microscopical examination the 
diameter of the fibres is increased, sometimes considerably, though not 
uniformly. The transverse striation is unaltered and the muscle nuclei 
are in some cases enlarged. The cause of the change is unknown. 

Atrophia Musculorum lipomatosa (Pseudo-hypertrophy of the Muscles).— 
In some cases, hand -in -hand with the production of new connective tissue 
in the muscles and the atrophy of the muscle fibres, or after these changes 



4 "[-l 






a 

- 1 



tea 



^^ ,^ ^ '^:: %J^ 



^ ^^ 



i \^ *'." , * ■'.?* "i'**-.-^-,--^ 









r--^ 



^ ^^ 



^ ^v ^v t,;* t\ 



Fig; 404.— progressive Muscular Atrophy (Soleus muscle, transverse section) . 

a, Increased interstitial tissue ; b, nearly normal muscle fibres : c, degenerated muscle fibres ; cZ, atrophied, 
muscle fibres ; e, clusters of proliferated muscle nuclei. 

have made considerable progress, there occurs a development of fat 
tissue between the fibres (Fig. 405) which may prevent any apparent 
diminution in the size of the muscles, or in some cases may even give 
them the appearance of a great increase in size. This condition is of 
most frequent occurrence in children, and is most apt to appear in the 
gastrocnemii muscles. In the upper extremities the deltoid and triceps 
are most frequently involved. The lesion may be symmetrical, affecting 
similar muscles on both sides of the body, or it may be unilateral. Parts 
of muscle bellies may be affected. 

The cause of this form of atrophy is not definitely known. Various 
lesions of the spinal cord have been described as occurring with it ; but, 
44 



690 YOLUNTARY MUSCLE. 

in many cases at least, alterations of the nerYOus system cannot be 
detected. The AYriter has described a case ' in which this lesion was 
marked in the gastrocnemii in connection with multiple false neuromata. 

DEGENERATION. 

Albuminous Degeneration of striated muscle occurs as a mark of toxae- 
mia in acute infectious diseases, and may lead to fatty degeneration. 







m^f<y^Miimmm^-^'rF&. 




Fig. 405.— Pseudo-Hypertrophy of Gastrocnemius Muscle (Fatty Infiltration). 
The specimen is from the case mentioned above, accompanying multiple neuroma. 

Fatty Degeneration, with greater or less destruction of the muscles, 
may commence with a simple swelling and fine granulation of the fibres. 
As the process goes on, smaller and larger fat droj^lets appear in the con- 
tractile substance, which loses its striations and becomes friable, and may 
be entirely destroyed, leaYing within the sarcolemma a mass of fatty 
detritus which may finally be absorbed and disappear. This alteration 
may occur in acute parenchymatous myositis in connection with Yarious 
forms of atrophy, in prolonged exhausting diseases, and in phosphorus 
poisoning. 

Hyaline Degeneration. — Under a Yariety of conditions the muscle fibres 
undergo a series of changes, leading to their couYcrsion into a trans- 
lucent, highly retractile material, somewhat resembling amyloid but not 
giYing its micro -chemical reactions, and apparently more nearly allied to 
hyaline material. The lesion in the muscle which we are considering is 
often called icaxy degeneration, from the peculiar appearance which the 
muscles present. When the lesion is far adYanced and extensive the 
muscles are brittle and have a grayish-yellow, translucent appearance. 
Microscopical examination of various stages of hyaline degeneration of 
muscle shows that the contractile substance of the fibres becomes at first 
swollen and granular, and gradually converted into hyaline material which 
may present the outlines of the swollen fibres, but is more frequently 

' Prudden, American Journal of Medical Sciences, July, 1880, p. 134. 



YOLUNTAEY MUSCLE. 



691 



broken into larger and smaller shapeless chimps (Fig. 406), which may 
disintegrate and finally be absorbed. Hand-in-hand with these changes 
there nsually occurs an increase in the interfibrillar connective tissue, 
and in certain cases there may be a proliferation of the muscle nuclei 
and a new formation of variously shaped cells within the sarcolemma 
which leads to the regeneration of the fibres. As a result of the brittle- 
ness of the degenerated muscles they are apt to rupture, and in this way 
haemorrhage may occur. 

This form of degeneration may occur in progressive muscular atrophy, 
in various infectious diseases, in trichinosis, with local inflammation, 
injuries, freezing, etc. It is, however, most marked and frecjuent in 
typhoid fever. In this disease the rectus abdominis and the abductors 
of the thigh are most frequently affected. 

Exx^eriniental investigations have shown that, under certain condi- 
tions, very similar appearances may be produced in the muscles by j)0st- 
mortem changes. Various changes — some of them necrotic — are at pres- 
ent included under the name hyaline degeneration of the muscles. 

True amyloid degeneration is rare. 

Soen has described a peculiar degeneration with atrophy of the stri- 
ated muscle of the uvula, in which a series of bleb -like structures form 
along the fibres, which they may finally replace. ' 

Calcification of muscle is of rare occurrence. 

Serous or Hydropic Infiltration of muscle fibres occurs under various 
conditions in association with other lesions. Larger and smaller spaces 




Fig. 406.— Hyaline Degeneratiox (So-called Waxy Degeneration) of Abdominal MrscLE in 

Typhoid Fever. 

filled with clear fluid are present between the fibres and often over small 
areas largely replacing them. Such fluid -filled spaces are often called 
vacuoles. 

INJURIES, H-ffiMORRHAGE, AND INFARCTION. 

Wounds and Rupture, — When the muscle fibres are severed by wounds 
or rupture there is more or less degeneration of the divided fibres, and 
the wound may heal by the production of granulation tissue, which grad- 
ually becomes converted into cicatricial tissue, thus binding the severed 
parts together. In some cases there is a moderate new formation of 
^Hoen, Jour. Exp. Med., vol. iii., p. 549, 1895. 



692 VOLUN^TAEY MUSCLE. 

muscle fibres (see page 100). Wlien the wound does not gape, so that 
the severed ends are not much separated, there may be, it would seem, 
a direct re-establishment of muscular continuity by new development 
of muscle, without the formation of much new connective tissue. 

Haemorrhage. — This may occur as a result of mechanical injury; from 
mixture of the fibres by convulsive contraction, as in tetanus ; or it may 
occur when the muscle fibres are degenerated, as in typhoid fever ; or in 
connection with certain general diseases, as scurvy, puri)ura, hgemor- 
rhagic diathesis, septicsemia, etc. The blood is usually readily absorbed. 

Embolic Infarction of Muscles in connection with heart disease has been 
described in a few cases, but it is rare. 



INFLAMMATION. (Myositis.) 

Suppurative Myositis. — In the early stages of this lesion the muscle is 
hypersemic and oedematous, and the interstitial tissue more or less infil- 
trated with small spheroidal cells. If the inflammation becomes intense 
there may be an excessive accumulation of pus cells, either diffusely in 
the interstitial tissue or in larger and smaller masses. Hand-in-hand 
with this cell accumulation occur degenerative changes in the muscle 
fibres. By pressure their nutrition is interfered with and they undergo 
granular, fatty, or hyaline degeneration and necrosis. They may com- 
pletely disintegrate ; or gangrene may occur, so that larger and smaller 
masses of the infiltrated muscle tissue become soft, foul-smelling, and 
converted into a mass of detritus in which but little muscle structure can 
be detected and which is intermingled with bacteria. In other cases 
there may be larger and smaller abscesses formed in the muscle, the 
muscle tissue itself degenerating and disintegrating and mixing with the 
contents of the abscess, or being x)ressed aside and undergoing atrophy 
and degeneration. In some cases, when the formation of pus is moderate 
in amount, there may be restoration by formation of granulation tissue 
between the muscle fibres. This becomes gradually dense and firm, and 
leads to more or less atrophy of the muscle fibres by pressure. 

Acute suppurative myositis may accompany wounds ; it is very com- 
mon in acute phlegmonous inflammations of the skin and subcutaneous 
tissue, and often accomj)anies acute infectious diseases, such as pyaemia, 
erysipelas, etc. In most cases the " pyogenic ^^ cocci are present in the 
inflammatory foci. Sux^puration not infrequently occurs in the muscles 
adjacent to the inflamed mucous membranes in diphtheria. 

Chronic Interstitial Myositis. — In this lesion there is a new formation 
of connective tissue between the muscle fibres or bundles of fibres. This 
new issue is sometimes very cellular, resembling granulation issue, and 
this probably represents an early stage of the disease. In other cases 
(Fig. 407) dense cicatricial tissue crowds the muscle fibres apart, induc- 
ing atrophy in them, and sometimes leading to their complete destruc- 
tion. This lesion, the analogue of chronic interstitial inflammation of 



VOLUNTARY MUSCLE. 693 

the internal organs, may occur in muscles which are adjacent to other 
parts which are the seat of chronic inflammatory processes. It may 
occur in muscles which are not used. The new formation of fibrous tis- 
sue seems in some cases to be secondary to atrophy of the muscle fibres. 
In this case it would more appropriately be called replacement fibrous 
lujperpJasia. 

Myositis Ossificans. — Under conditions and for reasons which we do 
not understand, there occasionally occurs, usually in young persons, a 
new formation of bone in the interstitial tissue of muscles, and in ten- 
dons, ligaments, fasciae, and aponeu- 
roses. This sometimes a^^parently '~" -_:,^ :- ^ 
starts as outgrowths from the perios- " :.: ^ "_ : =■ 
teum, sometimes not. The bone for- '^_^.. 1:'^'--;^ 
mations are apt to commence about -^.„_. ^ ' ^"^ " _ ^^:' ^ 
the neck and back, and may become ^^^ __-<-— ? \-:^j.,,^_ _ :^^ 
very widespread over the body. So T^^ . ..=" 
far as the muscles are concerned, :-' -i__r^y ^^^z"^^ - -^^^ 
there is usually an increase of con- --" ^ ~ ' '" ^ ^^ ^i 
nective tissue between the fibres and ,.~~ ^^J" -:- .,2^^ '- < 
bundles, in which new bone is formed, -^ i;^ 

usually in elongated and sometimes >-^^ :^_^-- --^— v^: 

in spicula-like masses. The muscle ne. 4or.-CHRONic intkrstitial myositis. 
fibres undergo secondarily a greater 

or less degree of atrophy or degeneration. There may be fatty infiltra- 
tion between the fibres, and various deformities are produced by the 
shortening and progressive immobility of the affected parts. 

While the above disease is a progressive and frequently a general one, 
there may be new formation of bone in muscle as a result of prolonged 
or repeated mechanical irritation. Thus in the adductors of the thigh 
in persons who are constantly in the saddle, or in the deltoid muscle of 
soldiers who strike this part with their weajDons in drill, there may be a 
formation of bone. ^ 

Tubercnlous and Syphilitic Inflammation in the muscle is of occasional 
occurrence ; the active processes are in the connective tissue and blood- 
vessels, the muscle fibres being secondarily involved in various phases 
of atroi^hy and degeneration. 



TUMORS. 

The tumors of the muscles usually develop in the connective tissue. 
Fibroma, chondroma, lipoma, myxoma, sarcoma may occur as primary 
tumors. Carcinoma and sarcoma may occur secondarily in the muscles 
as a result of local extension from adjacent parts. The muscle fibres 
are, as a rule, only secondarily affected by pressure, etc. , in tumors of 

Consult for a study of myositis ossificans De Witt, Am. Jour. Med. Sciences, vol 
XX., p. 295, bibliography. 



694 YOLUNTAEY MUSCLE. 

the muscles, but there exist observations which poiut to the possibility 
of a proliferation of the muscle nuclei and the new formation from them 
of cells which may take part in the growth of the tumor. 

PARASITES. 

Trichina spiralis is the most common parasite in the muscles. 
Cysticercus cellulosae and Echinococcus occasionally occur. 



CHAPTER XIV. 

THE NERVOUS SYSTEM. 

The Membranes and the Ventricles. 

THE DUE A MATEE CEEEBEALIS. 

The dura mater is a dense connective-tissue membrane which serves the double 
purpose of a periosteum for the inner surface of the cranial bones, and of an investing 
membrane for the brain. It is itself but poorly supplied with blood-vessels, but it con- 
tains the large venous sinuses which carry the blood from the brain. Lesions of the 
dura mater, therefore, are apt to be associated with lesions of the cranial bones, of the 
pia mater, or of the venous sinuses. 

In young children the dura mater adheres closely to the inner surface of the cranial 
bones, in adults it is more readily detached, and in old persons it is again more adher- 
ent. Chronic inflammation of the external layers of the dura mater also renders it more 
adherent to the bones, 

HEMORRHAGE. 

Extravasated blood may lie between the dura mater and the cranial 
bones, in the substance of the membrane, or between the dura mater and 
the pia mater. 

Hsemorrhages between the dura mater and the pia mater occur with 
chronic pachymeningitis, or from the vessels of the pia mater. Those 
in the substance of the dura mater are usually small. 

Haemorrhages between the dura mater and the cranial bones are usu- 
ally due to blows and injuries of the head, are often of considerable size^ 
separating the membrane from the bones, and may compress the brain. 
They are often associated with laceration of the brain, and hsemorrhages 
between the dura mater and pia mater. 

Pressure on the head of the infant in delivery may cause extravasa- 
tions of blood between the bones and the pericranium, as well as between 
the bones and the dura mater. 

THROMBOSIS. 

Thrombosis of the venous sinuses is not uncommon. It is often associ- 
ated with inflammation of the dura mater and with injuries and inflam- 
mations of the brain and pia mater, of the cranial bones, of the middle 
ear, and of the scalp. Like thrombosis in other parts of the body, it 



696 



THE XERYOUS SYSTEM. 



may occur in the infectious and exhausting diseases. It may occur in 
apparently healthy iDcrsons without discoverable cause. The thrombi 
may be red or white and firm. They may induce no secondary changes, 
or they may extend into the Ycins and induce hsemorrhagic softening of 
the iuYoh ed areas of the brain. 



INFLAMMATION". (Pachymeningitis.) 

This may involYe the external layers of the membrane, pachymenin- 
gitis externa, or the internal layers, jyachymeningitis interna. It may be 
either acute or chronic. The tissues of the substance of the dura mater 
participate to a greater or less degree in these changes, but the chief 
lesions are upon the surfaces. 

Acute pachymeningitis externa is usually secondary to injuries or dis- 
eases of the cranial bones ; thus it may be incited by fractures of the 




Fir. 408.— Pachymeningitis Interna H^,morrhagica— Chronic. 
Ai the left near the vessels are connective-tissue cells containing blood pigment. 



skull, either depressed or not, osteitis, caries, suppuratiYC inflammation 
of the internal and middle ear and mastoid cells. The dura mater is com- 
monly congested and swollen, and may contain small ecchymoses. The 
inflammation is usually suppurative, and pus may accumulate between 
the membrane and the bone, or in the substance of the membrane. The 
areas of inflammation are not usually extensiYC. It sometimes leads to 
thrombosis of the Yenous sinuses, and sometimes gangrene of the dura 
mater occurs. The inflammation may extend to the inner surface of the 
dura mater, to the pia mater and brain, or it may remain localized and 
undergo resolution. 

Acute pachymeningitis interna may be secondary to inflammation of the 
external surface, or it may occur as a complication in pyaemia, puerperal 
fcYer, chronic diffuse nephritis, in the exanthemata and erysipelas, or 
independently. There is a general or circumscribed production of fibrin 




THE NERVOUS SYSTEM. 697 

and pus, so that the internal surface of the membrane is lined with a 
laj'er of soft, yellow exudate. 

Simple chronic pachymeningitis consists in the formation of new con- 
nective tissue in the dura mater, by which it becomes thicker and in 
many cases abnormally adherent to the bones of the skull. This thick- 
ening may be general or circumscribed, and may involve the entire 
thickness of the membrane. Xot infrequently, when the external layers 
are especially involved, firm adhesions to the skull occur, with ossifica- 
tion of the outer layers, so that shreds of the membrane containing little 
masses of bone (osteophytes) remain sticking to the skull when the mem- 
brane is strix)i3ed off. 

Pachymeningitis Interna Hsemorrhagica, — This is an important form 
of chronic inflammation of the internal layer of the dura mater, charac- 
terized by the formation of layers of new deli- 
cate connective tissue with numerous very thin- 
walled blood-vessels from which the blood is 
prone to escape. The membrane may at first 
appear as a delicate fibrinous pellicle, with small 
red spots scattered through it, or it may look 
like a simple reddish or brown staining of the 
inner surface of the dura mater. Microscopical ^ .nn ^ o 

^ Fig. 409.— Brain Sand from 

examination shows this membrane to consist of pachymenixgitis interna. 
numerous blood-vessels, mostly capillaries with 

very thin walls, which may be distended or pouched, and which have 
grown out from the vessels of the dura mater (Fig. 408). Between 
the vessels is a homogeneous or slightly differentiated basement sub- 
stance, containing a variable number of spheroidal, fusiform, or branch- 
ing cells. Eed blood cells in variable quantity, and blood pigment in 
various forms, frequently enclosed in the new cells, and small calcareous 
concretions (brain sand) (Fig. 409), also lie in the intervascular spaces. 
In more advanced stages the new membrane may become greatly thick- 
ened, its outermost layers being changed into dense fibrous tissue with 
obliteration of the vessels ; while the more recently formed layers are 
similar in structure to those at first developed. Considerable blood usu- 
ally escapes from the vessels of the new membrane by diapedesis, in all 
stages of its formation, and the vessels are also very liable to rupture, 
giving rise to extensive haemorrhages either into the substance of the 
membrane or between it and the pia mater. Sometimes masses of new 
tissue and blood, from half an inch to an inch or more in thickness, are 
in this way formed, greatly compressing the brain. These new mem- 
branes are most frequently formed over the convexity of the brain, but 
may extend over nearly the entire surface of the dura mater. Some- 
times, when old, the entire membrane, densely pigmented and firm, 
lies loosely beneath the dura mater without compressing the brain or 
giving any clinical indication of its presence. The membrane may in- 
duce chronic changes in the pia mater, with or without accompanying 
changes in the cortical portion of the brain. 



698 THE NERVOUS SYSTEM. 

Earely, serum accumulates between the layers of the new membrane, 
and in this way cysts of large size may be formed. In rare cases diffuse 
suppuration of the entire new membrane occurs. 

The slighter degrees of this form of inflammation may occasion no 
symptoms during life. They are not infrequently found in persons suf- 
fering from various chronic brain lesions and from chronic alcoholism, 
but they may occur unassociated with complicating lesions. The more 
advanced forms of the lesion are frequently found in idiots, epileptics, 
etc. 

Tuberculous pachymeningitis may occur secondarily to that form of in- 
flammation in the pia mater or the bones, or as a part of general miliary 
tuberculosis. The tubercles may be situated on either surface of the 
membrane or in its substance, and may be single or aggregated, forming 
large masses. 

Syphilitic pachymeningitis manifests itself by the formation of so-called 
gummy tumors up6n either the external or internal surface of the dura 
mater. These tumors may be single or multiple, and vary greatly in 
size. They may be accompanied by simple inflammatory changes in the 
dura mater in their vicinity. They may undergo suppuration with the 
formation of abscess ; the inflammation may extend to the pia mater, 
inducing simple or syphilitic meningitis and adhesions between the dura 
mater and pia mater. The gummata may, on the other hand, when occur- 
ring on the outer surface of the membrane, cause absorption and perfo- 
ration of the bones of the skull. 

TUMORS. 

Fibromata and Lipomata occur rarely in the dura mater and are of 
small size. 

Small Chondromata are sometimes found connected with the dura 
mater at the base of the brain. 

Osteomata, — In addition to the formation of osteophytes in chronic 
external pachymeningitis, plates and, more rarely, globular masses of 
bone may be formed in the dura mater, unconnected with the bones 
of the skull. They are most frequently found in the falx cerebri, but 
may occur elsewhere. The new bone may be dense or loose in texture, 
and usually produces no symptoms. 

Endotheliomata.' — These tumors may grow inward or outward, causing 
pressure on the brain or absorption and perforation of the bones ; they 
often attain considerable size. Some of these tumors somewhat resemble 
certain forms of epithelioma, and have often been described as primary 
carcinomata. 

Sarcomata are the most common tumors of the dura mater, and of 
these the spindle -celled forms are of more, the round- and polyhedral- 
celled of less frequent occurrence. They may grow from either surface 

^ For a consideration of tumors of the dura mater allied to the endotheliomata con- 
sult Dagonet, Arch, de Med. exp., May 1st, 1892. 



THE NEHYOUS SYSTEM. 699 

of the membrane. Some of the round- and polyhedral-celled forms are 
soft and very vascular, and are apt to involve the neighboring pia mater 
and brain tissue, or the bones of the skull, which they may perforate. 
They sometimes project through the opening in the skull in fungous, 
bleeding masses. 

Psammomata are small globular tumors, often multiple and jiedicu- 
lated, growing from the inner surface of the dura mater. They are usu- 






,'■4. « ' f , 'f> Vi 

m^' 



3V ">, ^^^ ■*?, 




Fig. 410.— psammoma op the Dura Mater. 

ally composed of tissue fibrous, sarcomatous or endotheliomatous in char- 
acter, and contain variously shaped calcareous concretions similar in 
appearance to the so-called brain sand ' (Fig. 410). 

THE PIA MA TUB CEBEBRALIS. 

General Characters of the Pia Mater. 

The external surface of the brain is invested by a connective-tissue membrane 
which covers the convoiutions, dips down into the sulci, and extends into the ventricles. 
This membrane is abundantly supplied with blood-vessels, and from it numerous ves- 
sels extend into the brain, so that any disturbance in the circulation of the blood in the 
pia mater involves a disturbance in the circulation of the blood in the brain also. 

The connective tissue which makes up the pia mater is arranged in a series of mem- 
branes and fibres reinforced by elastic tissue, so arranged as to form a spongy membrane 
containing numerous cavities more or less filled with fluid. These cavities are continu- 
ous with the perivascular spaces which surround the vessels that pass from the pia mater 
into the brain. The outer laj^ers of the pia mater are the most compact, and are covered 
on their outer surface by a continuous layer of endothelial cells. This external layer 
of the pia mater is often described as a separate membrane called the "arachnoid," but 
it is really only part of the pia. The deeper layers of the pia contain the blood-vessels. 
The membranes and fibres which compose the pia mater are partly coated with cells 
which have irregular and delicate cell bodies and large, distinct nuclei. 

Along the borders of the longitudinal fissure, and, more rarely, on the under sur- 
face of the brain, are a number of small, white, firm, irregular bodies, the Paccliionian 
bodies. They vary in their size, their number, and in the extent of the surface of the 
hemispheres which they cover. They may perforate the dura mater, or, more rarely, 
the wall of the longitudinal sinus, and may produce erosions of the skull bones. They 
are composed of fibrous tissue and may undergo fatty or calcareous degeneration. 
As they are so commonly found and are not known to be of any pathological signifi- 

^For a study of psammoma consult Ernst, "Ueber Psammoma," in Ziegler's Bei- 
trage zur path. Anatomic, Bd. xi., p. 234, 1892. 



700 THE NERVOUS SYSTEM. 

cance, they may almost be regarded as normal structm'es; at any rate, we do not know 
what causes them or their variations in size and number. 

The pia mater is frequently thickened, opaque, and white, either in diffuse patches 
or, more commonly, along the course of the vessels. In other cases single or multiple 
small Avliite spots, of the size of a pin's head or smaller, may be seen in the membrane, 
not appreciably elevated above the surface, but due to localized thickening. These 
slight opacities of the pia mater are commonly believed to be dependent upon repeated 
congestions of the membrane or upon chronic meningitis,' but there is no evidence that 
this is always the case. They are most frequently found in old persons, but ma}^ exist 
at any age, and do not necessarily indicate the pre-existence of disease, although similar 
appearances are common in the chronic insane and in drunkards. 

The amount of blood contained in the vessels of the pia mater after death varies 
greatly, and is by no means a reliable indication of the amount present during life. In 
general anaemia the vessels of the pia mater may contain little blood, but, on the other 
hand, they sometimes seem to contain a relatively larger amount than other parts of the 
body. In oedema of the brain and pia mater the vessels of the latter may contain but a 
small amount of blood. 

(EDEMA. 

The quantity of serum beneath the pia mater and infiltrating its tis- 
sue is very variable in amount. It may accumulate as a result of atrophy 
of the brain substance or of venous hypersemia, and sometimes is, and 
sometimes is not, accompanied by oedema of the brain substance. It 
may be diffuse or localized. It is not infrequent to find in hospital pa- 
tients suffering from chronic nephritis, cardiac or pulmonary disease, or 
chronic alcoholism, a very considerable amount of serum in this situa- 
tion, and yet the patient has been free from cerebral symptoms. In 
other cases a serous effusion may accompany grave cerebral symptoms. 
It is necessary to be very careful in judging of the importance of this 
accumulation of fluid, especially in determining the cause of death in 
the absence of other marked lesions (see page 722). 

It should always be borne in mind that an accumulation of fluid be- 
neath and in the meshes of the pia mater may occur as a result of post- 
mortem changes. 

HYPERiEMIA AND HAEMORRHAGE. 

Hypersemia, — The pia mater may be hypersemic in early stages of men- 
ingitis, after death from delirium tremens or following epileptic convul- 
sions ; in infectious diseases, and poisoning. It may be due to the pressure 
of exudates or tumors on the veins, or to general or local lesions of the 
circulatory system. The time which elapsed between death and. the au- 
topsy, the position in which the body has lain, the coagulability of the 
blood may have an important bearing upon the amount and situation of 
blood in the pia. 

Hsemorrhage. — This may occur either into the space between the dura 
mater and the pia mater — inter meningeal hdemorrhage — or in the meshes of 
the pia or between the latter and the brain. It may be due to injury, 
to rupture of aneurisms or otherwise diseased blood-vessels, to throni 
boses of the venous sinuses, or to conditions which we are unable to as- 



THE NERVOUS SYSTEM. 701 

certain. Haemorrhages without known cause not infrequently occur in 
the substance of the pia mater in young children, but in adults they are 
apt to be the result of injury. Multiple ecchymoses, however, in the 
substance of the pia mater sometimes occur in infectious diseases and 
also in acute inflammation of the pia mater. Haemorrhages in the brain 
substance may lead to the accumulation of blood beneath or in the 
meshes of the pia mater. Intermeningeal haemorrhage in infants as a 
result of injury during birth is not uncommon. Small, and sometimes 
considerable, extravasations of blood may occur from diapedesis, and 
sometimes, as a result of chronic congestion, degenerated blood pigment 
collects along the walls of the vessels. The extravasated blood in menin- 
geal hgemorrhage, if small in quantity, may be largely absorbed, leaving 
a greater or smaller accumulation of pigment at the seat of the haemor- 
rhage. Such pigmentations may last for a long time. 

INFLAMMATION. (Mening-itis— Leptomeningitis.) 

We distinguish acute, chronic, tuberculous, and syphilitic meningitis. 

Acute Meningitis may occur as the characteristic lesion of epidemic 
cerebro -spinal meningitis ; it is a not very infrequent complication of 
pneumonia, typhus and typhoid fever, the exanthemata, and of chronic 
diffuse nephritis; it may be secondary to injuries and inflammation of 
the cranial bones, of the dura mater, and of the middle ear, and it some- 
times occurs as an independent infectious process (see page 194). 

In acute meningitis the inflammatory process is apt to extend down- 
ward and involve the pia mater of the cord. It may also involve the 
ependyma of the ventricles, and cause the distention of these cavi- 
ties with serum. This latter condition is especially frequent in young 
children. 

It is convenient to consider two varieties of acute meningitis, one in 
which there is cell proliferation with little or no exudate, the other in 
which exudate is present. In many cases at least the first may be the 
early stage of the latter form. 

1. Acute Cellular Meningitis. — The pia mater is congested, its 
surface is dry and lustreless, and it is somewhat opaque. The changes 
in the gross appearance of the membrane are not marked and are easily 
overlooked, but the minute changes are more decided. There is a pro- 
liferation of the endothelial and connective-tissue cells of the pia, and 
often a moderate collection of fluid and leucocytes in the meshes of the 
pia. This ceil proliferation may involve the pia mater over most of the 
surface of the brain. This form of meningitis is of frequent occurrence 
and is attended with the ordinary clinical symptoms of acute meningitis. 

2. Acute Exudative Meningitis is characterized by the accumu- 
lation, chiefly in the meshes of the pia mater and along the walls of the 
blood-vessels, of variable quantities of serum, fibrin, and pus. Some- 
times one, sometimes another of these preponderates, giving rise to ser- 
ous, fibrinous, or purulent forms of the inflammation. The absolute 



702 THE NERVOUS SYSTEM. 

quantities, too, of the exudations vary greatly. In some cases death 
may occur with so slight a formation of exudate that to the naked eye 
the pia mater may look quite normal or perhaps only moderately hyper- 



^ <^ 



Fig. 411.— Acute Exudative Meningitis. 



Showing distention of the meshes of the pia mater of the brain with fluid, in which are leucocytes and ex- 
foliated endothelium, the lattejr undergoing proliferation. 

semic or oedematous ; the microscope, however, in these cases will reveal 
pus cells in small numbers and new-formed connective -tissue cells (Fig. 
411 and Fig. 412), and sometinies flakes of fibrin in the meshes of the 
pia and along the walls of the vessels. In other cases turbid serum in 
the meshes of the membrane is all that can be seen, and the microscope 
shows the turbidity to be due to pus cells or a small amount of fibrin. 
Again, either with or without marked oedema of the pia mater, yellow- 
ish stripes are seen along the sides of the veins, sometimes appearing like 
faint turbid streaks, and at others dense, opaque, thick, and wide, and 
almost concealing the vessels. These are due to the accumulation of 
pus cells and fibrin in large quantities along the vessels, and they are best 
seen and most abundant around the larger veins which pass over the 



-^ :,"a « 


%l 








^'^ 




^ ^ 


a 















y:) zr 




: 


© 
"' 








3^ 


v.? 




. % « 


»'''o^2^ 




^ 


^ 




y 



Fig. 413.— Acute Exudative Meningitis. 

Proliferation of connective -tissue cells and extravasation of leucocytes in the adventitia of a small blood- 
vessel of the pia mater. 

sulci. In still other cases the infiltration with pus and fibrin is so dense 
and thick and general that the brain tissues, convolutions, and most of 
the vessels of the pia mater themselves are concealed by it. This pus is 
usually of a greenish -yellow color, and is sometimes so thick as to form 



THE XEEYOUS SYSTE3I. 703 

a sort of cast of the brain surface at the seat of the lesion (Fig. 413). 
Sometimes extra vasated red blood cells are mingled with the other exu- 
dations, as the result of diapedesis. Microscopical examination shows 
numerous white blood cells sticking in the walls of the veins and capil- 
laries, or the vessels may be blocked with them. It is evident that a 
large part of the pus cells accumulates as the result of emigration. The 
connective-tissue cells of the pia mater may be detached from their 
places or degenerated. In some cases there are considerable accumula- 
tions of pus between the pia mater and the brain substance and along 
the A essels which enter the latter. More rarely pus is found upon the 
free surface of the membrane. The brain substance may be compressed 
by the accumulated exudate, so that the convolutions are flattened. 
The cortical portion of the brain may be simply infiltrated with serum 



Fig. 413.— Acute Exudative Meningitis. 

a. Convolutions of cerebrum ; h, pia mater thickly infiltrated with pus; c, blood-vessels entering brain 
from pia and surrounded by a zone of pus cells ; f?, congested blood-vessels of pia mater ; e, smaller blood- 
vessels of pia, around wliich pus cells are collected in dense masses. 

— oedematous — or it may undergo degenerative changes, or it may be 
the seat of punctate haemorrhages, ^ot infrequently the inflammation 
extends to the ventricles, which may contain purulent serum, and to the 
pia mater of the cord. This form of inflammation is most frequent on 
the convexity of the brain, but may extend or even be confined to the 
base. It may be localized, but frequently extends widely over the sur- 
faces of the hemispheres. 

^\Ti3n recovery from acute exudative meningitis occurs there may be 
fatty degeneration of the cells which have accumulated in the pia mater, 
particularly along the vessels (Fig. 414), and this may produce white 
patches in the membrane and threads along the blood-vessels, which 
resemble the appearance of an accumulation of exudate in the acute 
stage. Fatty degeneration of the blood-vessels and cells of the pia 
mater may also occur without acute inflammatory changes. 

Sometimes, in children and young adults, inflammatory changes in 



704 



THE NEEYOUS SYSTEM. 



the ventricles persist for days and weeks after the subsidence of the in- 
flammation of the pia mater. 

For a discussion of the bacterial excitants of exudative meningitis 
see page .195.' 

Chronic Meningitis. — Either the pia mater at the base of the brain 
alone may be inflamed (basilar meningitis), or the pia mater over the 
conYCxity alone, or the entire pia mater, or circumscribed patches of the 
membrane. The pia mater is thickened and opaque, the thickening 
being sometimes very considerable. There is a formation of new connec- 
tive tissue and this may be associated with accumulation of pus, fibrin, 
and serum ; the relative quantity of these inflammatory products varies 
in different cases. Firm and sometimes extensive adhesions may be 
formed between the dura mater and the j)ia mater. Not infrequently the 
cortical portions of the brain particiiDate in the process, and there is an 




Fig. 414.— Fatty Degeneratiox of Cells Along the Blood-vessels of the Pia Mater after 

Exudative Memngitis. 

From the pia mater of a child Ave years old. 



infiltration of small spheroidal cells around the blood-vessels, thickening 
of the walls of the vessels, and degenerative changes and atrophy of the 
nerve tissue. New connective tissue may also form in the brain sub- 
stance, which may become closely adherent to the pia mater. The ven- 
tricles of the brain also may contain an increased amount of serum and 
may be dilated ; the ependyma may be thickened and roughened. This 
form of inflammation may be the result of injury or disease of the cra- 
nial bones, or secondary to chronic pachymeningitis or to inflammation of 
the brain substance. It may occur in the vicinity of tumors of the brain 
or meninges. It may be a complication of chronic diffuse nephritis or 
the result of chronic alcoholic poisoning. It may occur in marked form 
in general paresis of the insane. 

' The close topographic relationships which the nasal cavities and the middle ear 
bear to the meninges are signilicant in this connection on account of the possibility of 
the transmission to the brain membranes of bacteria not uncommonly present and usu- 
ally harmless in the former situations. 



THE NERVOUS SYSTEM. 



705 



Tuberculous Meningitis. — This is especially characterized by the forma- 
tion in the pia mater of miliary tubercles, associated with more or less 
well-marked exudative inflammation. It may occur in adults and in 
children, but is more common in the latter. The dura mater may be 
unchanged, or its inner surface may be sprinkled with miliary tubercles. 
The pia mater may or may not be congested ; it may look dry on the sur- 
face or it may be oedematous. Usually the brain seems to fill the cere- 
bral cavity to an unusual degree, and the convolutions are flattened. If 
the pia mater be oedematous the serum may be clear, or turbid with pus 
and fibrin. The membrane may present any of the general appearances 
of exudative meningitis. But always in addition to these, and some- 
times without them, miliary tubercles, either widely scattered or in great 
numbers, may be seen usually more abundant over the sulci than else- 
where. They are commonly more abundant at the base of the brain than 
on the convexity, and are frequently confined to the base. Some of the 
tubercles are so small as to be scarcely visible or entirely invisible to 
the naked eje; others are as large as a pin's head or larger. They are 
usually most abundant along the blood-vessels, but may occur elsewhere. 





':>\o- 



Fig. 415.— Miliary Tubercle of the Pia Mater of a Child. 

There is an area of caseation at the centre ; on the right of this are two giant cells ; there is a peripheral 
zone of small cells. The leucocytes are increased in the meshes of the pia. 



They may be formed in the membranous prolongations of the pia mater 
' which dip into the sulci, around the vessels which enter the brain sub- 
stance, in the choroid plexus and ependyma of the ventricles, and may 
exist in the spinal cord. 

The miliary tubercles have the usual structural characters of focal 
tuberculosis in connective tissue (Fig. 415). 

In children the ventricles are usually more or less distended by an 
accumulation of transparent or turbid serum, and the walls of the ven- 
tricles may be studded with miliary tubercles (see Fig. 416). In adults 
the ventricles are less frequently involved. The brain tissue around 
the ventricles is often softened. The central canal of the spinal cord 
may also be dilated. It is the dilatation of the ventricles which causes 
the flattening of the convolutions, and the flattening is usually in direct 
proportion to the amount of accumulated fluid. 

Owing to the frequency of the dilatation of the ventricles with serum 
in children, the disease is often called acute hydrocephalus. 

In both children and adults the tuberculous inflammation may produce 
large masses of tuberculous tissue, which undergo cheesy degeneration, 
in the pia mater and the brain tissue. 
45 



706 THE NERVOUS SYSTEM. 

In almost all cases of tuberculous meningitis there is tuberculous 
inflammation in other parts of the body. 

Miliary tubercles in the choroid of the eye are present in a considerable 
proportion of cases. 

The cortex of the brain may be hypersemic, and punctate haemor- 
rhages may be present in the cortex and in the pia mater. 

Syphilitic Meningitis. — In this form of inflammation, which is usually 
circumscribed, there is a development of gummy tumors of variable size, 
frequently associated with simple inflammation of the membrane, either 






Fig. 416.— a Miliars Tubercle of the EPE^DYMA of the Lateral Ventricle. 
This shows an early stage of tubercle formation on the ependyma without marked caseation. 

with the formation of serum, fibrin, and jdus, or with the development of 
new connective tissue and the consequent thickening of the membrane. 
The gummata may form in the pia mater covering the convexity, or at 
the base of the brain. They may grow outward, involving the dura 
mater; or inward, encroaching upon or involving the brain tissue. 
Although usually circumscribed, syphilitic inflammation may occur as 
a diffuse thickening of the membrane. The syphilitic nodules, includ- 
ing the gummata and new-formed connective tissue, are often very 
small, but may be as large as a hen's egg. 



TUMORS. 

Hsematoma. — In chronic pachymeningitis of long standing the new 
connective tissue may form large, flat cysts between the dura mater and 
the pia mater, which may compress the surface of the brain. The blood 
originally contained in these cysts may be absorbed and replaced by 



THE NERVOUS SYSTEM. 707 

serum, the attachments to the dura mater may disappear, and the whole 
appearance becomes that of an independent cyst between the dura mater 
and the pia mater. Fibroma, lipoma, myxoma, chondroma, and osteoma are 
of rare occurrence. 

Endotheliomata. — These tumors are of not infrequent occurrence, and 
may grow from the pia of the cerebrum or cerebellum or from the chor- 
oid plexus. They may be single or multii)le. They may be small or so 
large as seriously to compress the brain. 

Some of them are comj^osed of a connective-tissue stroma which en- 
closes regular spaces filled with large, flat, nucleated cells. These may 
resemble carcinoma. Some of them are composed of a connective-tissue 



•^;^v^ 

















Fig. 417.— Endothelioma of the Cerebellum Originating in the Pia Mater. 
Showing general appearance of the tumor (see Fig. 418) . 

stroma which forms cavities lined with cylindrical epithelium. In such 
tumors the stroma may grow so as to form papillae covered with cjdin- 
drical epithelium ; or in addition there may be mucous degeneration of 
tlie stroma. In some of them there is a connective -tissue stroma which 
contains large numbers of blood-vessels. Around these blood-vessels are 
arranged regular masses of polyhedral cells (Figs. 417 and 418). 

In some of them the stroma is scanty. The cells are numerous, large, 
flat, and arranged in little globular masses or nests. If in these little 
nests there is a deposition of the salts of lime, forming concretions like 
the so-called ''brain sand,'' the tumor is called a ''psammoma.'' Some 
of the tumors seem to be formed of very thin, nucleated membranes ar- 
ranged in concentric layers like the layers of an onion. 



708 THE NEEYOUS SYSTEM. 

Some of the tumors are composed of balls or nests of large, flat cells, 
with which are found crystals of cholesterin — '^cholesteatoma.^' ' 

Sarcoma. — Tumors belonging to the ordinary types of round- and fusi- 
form-celled sarcoma, and of myxo-sarcoma, are occasionally found in the 
pia mater. 

Cysts. — Small cysts are often found in the choroid plexus. Earely 
such cysts reach a larger size, even as large as a pigeon's egg. 



c—--- 



'SJ^ 



c^vS 



iS? 







- ^ % "^JU _ ^ 






m % ^ ^Q"^*. (s. ^* vv^ 



"l^^.^. tj^.^ . ^ ^^^^^ 



^t^ ^ „.. ^ ^'.^ % ^^w ^ ^.^© 



^ 



^ ©.-/^ 



Fig. 418.— Endothelioma of the Pia Mater of the Cerebellum. 

From specimen shown in Fig. 417 more highly magnified. A, Section of pia mater dipping into a sulcus; 
B, tumor cells growing at each side of the pia ; C, surface of cerebellar convolutions. 

Cysts of the pia mater containing serum, with walls and septa of con- 
nective tissue and compressing the brain, have been described. 

Variously shaped pigment cells not infrequently occur in the pia mater, 
either scattered or sometimes in considerable masses ; they seem to have 
little pathological significance, ^ot infrequently thin plates of new- 
formed bone are found in the pia mater, associated with a thickening of 
the membrane. 



PARASITES. 

Cysticercus has been observed in the pia mater. 

^ For a critical review of these and other pial tumors, with bibliography, see Bost- 
roem, Centrbl. f. allg. Path, ii. path. Anat., Bd. viii., p. 1, 1897. 



THE NERVOUS SYSTEM. 709 



THE DUE A MATEB SPINALIS. 

The dura mater spinalis, unlike that of the brain, does not serve as periosteum to 
the bones forming the cavity, so that the lesions of the two membranes differ somewhat. 



HAEMORRHAGE. 

Haemorrhage may occur, as the result of iujury, between the dura 
mater and periosteum, or it may occur in tetanus, as a result of circula- 
tory changes induced by muscular spasm, or in the asphyxia of new- 
born children. Small haemorrhages on the surfaces of the membrane 
may occur as the result of inflammation. 

Serous fluid may accumulate outside of the dura mater as a result of 
post-mortem changes, or in connection with circulatory or inflammatory 
changes in the membranes. 

INFLAMMATION. (Pachymeningitis.) 

Acute external pachymeningitis is usually secondary to disease or in- 
jury of the spinal column, and may result in collections of pus between 
the dura mater and periosteum, usually most abundant posteriorly. 
Haemorrhagic pachymeningitis occurs in the dura mater spinalis, with the 
formation of products similar to those observed in the brain, in the 
chronic insane and in drunkards. Simple chronic pachymeningitis interna 
with the formation of new connective tissue containing brain sand, is not 
infrequent. The new tissue may form minute projections of the surface, 
or, when more abundant, the psammomata. Tuberculous inflammation of 
the dura mater spinalis may occur in connection with tuberculous men- 
ingitis, or be secondary to tuberculous inflammation of the vertebrae. 

TUMORS. 

Fibromata, lipomata, chondromata, myxomata, endotheliomata, and adeno- 
sarcomata occur in the dura mater spinalis as primary tumors. Carci- 
nomata and sarcomata may occur as secondary tumors. Small plates of 
new-formed bone are rarely found in the dura mater spinalis. 

PARASITES. 

Echinococcus developing outside of the spinal canal may perforate the 
dura mater ; or the cysts may lie between the dura mater and the pia 
mater. 

THE FIA MATEB SPINALIS. 

It is difficult in most cases in the pia mater, as well as in the dura mater spinalis 
and in the spinal cord, to judge with certainty, from the appearances after death of 
the blood contents of the vessels, of these parts during life. The same is true of abnor- 



710 THE NERYOUS SYSTEM. 

mal quantities of serum found after death. The veins of the pia mater, especially in 
the posterior region, may be greatly distended with blood after death, without pre- 
existing disease; and the intermeningeal space may contain much fluid under the same 
condition. 

H-ffiMORRHAGE. 

Haemorrhages may occur from injury in connection Tvdth seYere con- 
vulsions, or general diseases such as the hsemorrhagic diathesis, scurvy, 
smallpox, etc. The haemorrhages under these conditions, except from 
injury, are not usually extensiYC. But in some cases of injury or 
cerebral apoplexy, from the bursting of aneurisms of the basilar or 
vertebral arteries, or in cases in which we cannot find a cause, a very 
large quantity of blood may collect between the dura and pia mater, 
and in the meshes of or beneath the latter. 



INFLAMMATION. (Meningitis.) 

Acute exudative spinal meningitis occurs under essentially the same 
conditions and with essentially the same post-mortem appearances as 
acute cerebral meningitis, though it is less frequent. The exudate is 
ai)t to be most abundant in the posterior portions. It may be asso- 
ciated with a similar inflammation of the pia mater cerebralis, and the 
inner surface of the dura mater may be involved. The disease may be 
circumscribed, but usually affects the entire length of the membrane. 

Chronic spinal meningitis is not infrequent, manifesting itself in the 
formation of larger or smaller patches of new connective tissue or thick- 
enings of the pia mater. The pia and dura mater may thus be firmly 
united in places by adhesions, or the pia mater may become closely ad- 
herent to the substance of the cord. 

Not very infrequently large numbers of pigment cells are found in 
the j)ia mater spinalis, sometimes giving it a distinct gray or blackish 
color. 

Tuberculous inflammation is usually most marked, when associated 
with a similar condition of the pia mater cerebralis, in the uj^per por- 
tions of the cord ; but it may extend over the entire membrane. The 
conditions under which it occurs and the character of the lesions are 
similar in both. 

TUMORS. 

Fibromata, myxomata, sarcomata, and endotheliomata have been found. 
Small plates of cartilage and bone (Fig. 419) are sometimes found in 
the pia mater. 

PARASITES. 

Cysticercus sometimes occurs in the meshes of the pia mater. 



THE NERVOUS SYSTEM. 711 

THE YENTBICLES OF THE BBAIX. THE EFENBYMA AND 

CHOBOIB BLEXrS. 

GENERAL CONSIDERATIONS. 

As the lymph -spaces of the pia mater paid the ventricles of the brain 
are in commnnication, it might be snx)posed that they would share alike 
in the accumulation of fluids. This, hoAvever, is not the case. The 
membranes of the brain may be highly oedematous while the ventricles 
contain about the normal quantity of fluid ; or, on the other hand, the 
ventricles may be widely dilated and the i)ia mater unusually dry. Many 
of these varying conditions maj^ be understood by remembering that the 
skull and spinal canal form a closed cavity, and that accumulations of 
fluid in one part must be at the expense of some material occupying 
other parts, either blood, serum, or brain tissue. It is not always easy 
to see, however, exactly how the compensation occurs. 

There may be an unusual amount of fluid in the ventricles of the 
brain as a result of post-mortem change ; in connection with senile or 




Fig. 419.— Plates of Bone ix the Pia Mater Spinalis. 

other atrophy of the brain, or in the general vascular changes which lead 
to oedema of the brain ; in connection with inflammation of the meniDges 
or of the ependyma ; or under conditions which we do not understand, 
as in some cases of congenital and acquired hydrocephalus. Accumula- 
tions of fluid in the ventricles are often called internal hydrocephalus to 
distinguish them from accumulations in the meninges — external hydro- 
cephalus. 

INFLAMMATION. (Ependymitis.) 

Acute Ependymitis. — In this condition, which may occur by itself, but 
is usually associated with inflammation of other parts of the brain, the 
ependyma is congested, the vessels are more prominent than usual and 
are often tortuous. The ependyma and the adjacent brain tissue may be 
thickened and infiltrated with pus cells, and the surface of the ependyma 
covered with fibrin and pus in variable quantity (Fig. 420). The cavi- 
ties of the ventricles may contain purulent serum. Small haemorrhages 
may also be present in the tissue of the ependyma. This, as well as 
other forms of inflammation, is more common in the lateral ventricles 
than in the others, but not infrequently involves the fourth ventricle. 
The choroid i^lexus may participate in the iDflammatory changes of the 



712 THE NERVOUS SYSTEM. 

ependyma. Tuberculous inflammation of the ependyma is, as above 
mentioned, a not infrequent accompaniment of tuberculoiis meningitis. 

Chronic Ependymitis. — This lesion, which is much more common than 
simple acute inflammation of the ependyma, occurs under a variety of 
conditions, and its nature and causation are in general very obscure. 
The ependyma is thicker, whiter, and more opaque than normal, so that 
the vessels may be nearly or quite invisible. The thickenings may oc- 






::'"v -•■#^ '^:v.^.^■• 



Fig. 420.— Acute Ependymitis. 

Showing replacement of the epithelium of the ventricle by inflammatory exudate ; collections of pus cells 
near the epithelium and about the adjacent small blood-vessels. 

cur in patches or diffusely, and the surface of the ependyma may be 
smooth, or roughened and granular. On microscopical examination the 
surface of the ependyma may be covered with the usual epithelium, but 
the new connective tissue which forms beneath it often raises it up in 
places, causing the roughness of the surface. The new tissue is usually 
rather loose in texture and may contain many small spheroidal cells ; but 
it may be dense in texture and contain few cells. The brain tissue be- 
neath the thickened ependyma may be softened or infiltrated with cells. 
The sides of the ventricles may be grown together in places by the adhe- 
sion of the thickened and roughened ependyma. The ventricles usually 
contain more serum than normal, and sometimes this accumulation is 
so great as to cause an enormous dilatation of them. While these are 
in general the prominent lesions in chronic inflammation of the epen- 
dyma, the cases vary greatly in the degree to which these changes are 
developed. 

The accumulation of fluid and the dilatation of the ventricles being 
the most marked feature in all this class of lesions, they are often called 
chronic hydrocephalus, but in many cases we have no evidence that the 



THE NERVOUS SYSTEM. 



13 



change in the ependyma is an important or even an actual primary 
factor. 

Hydrocephalus. — We may, for convenience of stncly, consider three 
classes of cases of hydrocephalus : first, congenital hydrocephalus in young 
children; second, secondary hydrocephalus in children and adults; third, 
primary hydrocephalus in adults. 

1. Congenital Hydrocephalus. — The lesion may be in an ad- 
vanced stage at the time of birth, or it may be scarcely evident or but 
moderately developed: It may progress rapidly and cause the early 
death of the child, or it may develop gradually or come to a standstill. 
In the more marked forms of the disease the ventricles are widely dilated 
(Fig. 421) and filled with serum, which is usually transparent. ]!^ot only 
the lateral ventricles, but also the third and fifth, may be involved ; the 
fourth is less apt to participate in the lesion, although it is sometimes 
dilated, as well as the central canal of the cord. 

The distention, especially of the lateral ventricles, may be so great 
that the brain tissue over the vertex is crowded up into a thin layer be- 
neath the dura mater, or it may be entirely destroyed. When the dila- 
tation of the ventricles is considerable, the convolutions ai^e flattened 
and may be almost entirely obliterated. The skull bones may be thin 
and bulging over the forehead and vertex; the fontanels and sutures 
widely open. The ependyma in these cases is usually thick and rough, 




Fig. 42L— COxVGenital Hydrocephalus in Child. About half natural size. 
a, a. Dilated lateral ventricles ; b, cornua, unequally dilated ; c, third ventricle ; c?, middle commissure. 



but it may be softened, and the blood-vessels may be dilated. The basal 
portions of the brain may be flattened, but are usually much less affected 
than the upper portions. The brain tissue is usually soft and ansemic. 

2. Secondaky Hydrocephalus. — This may occur in children and 
adults, and may be a result of epidemic cerebro- spinal meningitis, or of 
acute meningitis, or of chronic meningitis. It sometimes occurs in 
chronic alcoholic poisoning and in general paralysis of the insane. The 
amount of dilatation of the ventricles varies greatly in these cases, but 



714 THE NERVOUS SYSTEM. 

it is never so great as iu congenital hydrocephalus, and is not accomiDa- 
nied by the changes in the shape of the sknll which form so prominent a 
featnre in the latter disease, since the bones are firmer and the sntures 
united. In this form of chronic hydrocephalus the changes in the epen- 
dyma above described are usually more or less well marked, and they 
may be associated with the j)roduction of fibrin and pus. 

3. Primary Hydrocephalus in Adults.— The conditions leading 
to this form of lesion are not understood. It is apt to occur in persons 
over thirty years of age. Sometimes one, sometimes both lateral ven- 
tricles are dilated. The dilatation is usually moderate, sometimes very 
slight, and never as great as in congenital hydrocephalus. The ven- 
tricles usually contain transparent serum, and the ependyma is thickened 
and roughened. In some cases it is the only lesion found to account for 
the death of the patient. 

TUMORS. 

Xew formations of connective tissue in the ependyma, although usually 
diffuse, may be circumscribed and form small, projecting connective-tis- 
sue nodules, which may be reckoned among the fibromata. Small fibro- 
mata are sometimes detached from the walls of the ventricles and lie free 
in the cavity. Small lipomata, angiomata, and also sarcomata and glio- 
mata occur rarely. Chondromata and angiomata may occur in the choroid 
plexus, the latter sometimes being as large as a hen's egg. The choroid 
plexus is not infrequently the seat of transparent cysts, usually of small 
size ; they may contain a clear fluid, or colloid material, or droplets of 
fat, or calcareous particles. A small dermoid cyst containing hairs has 
been described. The cysts have no special pathological significance. 

Primary carcinomata sometimes involve the ventricles. 

The calcareous bodies called brain sand' (see Fig. 409), occur fre- 
quently in the choroid plexus, and corpora amylacea may occur here and 
beneath the ependyma. 

PARASITES. 

Cysticercus and echinococcus cysts are sometimes attached to the walls 
of the ventricles or may be free in their cavities. 



The Brain and Spinal Cord. 

Malformations of the Brain. 

Cyclopia. — This malformation consists in an arrest of development affecting the 
cerebrum, which, instead of separating into two hemispheres, remains single, with one 
venti'icle, and the rudiments of the eyes usually become joined and form one eye. This 
single eye is in the middle of the face, near the place of the root of the nose, in a single 

^ The little, hard masses called brain sand consist of aggregations of small particles 
of carbonate and phosphate of lime with a small amount of phosphate of ammonia and 
magnesium. With these there is more or less organic matter. 



THE NEEYOUS SYSTEM. 715 

orbit. Over this is an irregular body representing tlie nose. The rest of the face is 
well formed. The eyeball may be wanting entirely, or there are two eyes joined to- 
gether, or, more seldom, two separate eyes. The orbit is surrounded by rudiments of 
four eyelids. The frontal bone is single, the nasal bones are undeveloped ; the ethmoid, 
vomer, and turbinated bones are absent. The optic nerve is double, single, or absent. 
There may be hydrocephalus. Such children are incapable of prolonged existence. 

A^^EXCEPHALiA. — Tliis malformation may be of various degrees. The brain may 
be entirely absent, the base of the cranium being covered with a thick membrane, into 
which the nerves pass. The membranes may form a sort of cyst containing blood and 
serum, or portions of brain. Of the cranial bones, only those which form the base of 
the skull are present {acrania). The scalp is usually partl}^ or entirely absent over the 
opening in the skull; the eyes are prominent, and the forehead slopes sharplj^ back- 
ward. This malformation may occur in otherwise well-developed children. 

Hydrocephalus. — This lesion has been already considered above. It is proba- 
ble that in some cases hydrocepTiidus inter nns is due to a \)Y\masj x^avtial anencephalia, 
and that the accumulation of fluid is of secondary occurrence. In rare cases, only 
part of one lateral ventricle is hydrocephalic, giving to the head a protuberance on one 
side. The viability of the foetus depends upon the degree of the hydrocephalus. 
Hydrocephalus externiis is an accumulation of serum beneath the pia mater, or, according 
to some authors, between the pia and dura mater. It causes dilatation of the cranium 
and compression of the brain. It is of very rare occurrence, and may also be secondary 
to partial anencephalia. 

Cephalocele, or Brain Hernia. — When abnormal openings exist in the skull 
from malformation, the contents of the cerebral cavity are apt to protrude in the form 
of larger or smaller sacs. This may occur in cases of well-marked anencephalia or in 
cases in which the brain is well developed. The protruding sac formed of the meninges 
may or may not be covered with skin. If the contents of the sac are simply fluid, the 
lesion is called liydromeningocele ; if composed of brain substance, enceplialocele ; if the 
sac contain both fluid and brain substance, it is called liydr enceplialocele. The sacs may 
be very small or as large as a child's head. They may protrude from the top of the 
skull in acrania. They most frequently protrude through openings in the occipital 
bone, often hanging down in large sacs upon the neck ; also at the root of the nose, 
along the line of the sutures, at the base of the skull, and elsewhere. 

Microcephalia. — This is an abnormally small size of the brain, with a correspond- 
ingly small cranium. The diminution in size affects principally the cerebral hemi- 
spheres, though the other parts of the brain are also small. Thus the cerebellum may 
be of extremely small size. The cord may be smaller than normal, in which case the 
diminution in size is apt to show a direct dependence upon the cerebral lesions, the 
direct and the crossed pyramidal tracts being most affected. There may also be present 
imperfect development of the posterior columns and of the direct cerebellar tracts. The 
convolutions are few and simple, the cavities often dilated with serum ; on the mem- 
branes there may be traces of inflammation. The cranium is small, the face large, the 
rest of the body small. The malformation is in some cases caused by inflammation or 
dropsy of the brain during foetal life. It is endemic in some countries, buc single cases 
may occur anywhere. The foetus is viable. Absence or incomplete development of 
portions of the brain may occur, not only in idiots, but in persons w^hose minds are 
perfect. 1 

Malformations of the Spinal Cord. 

The malformations of the spinal cord may be conveniently classed as follows (Van 
Gieson^) : 

I, Congenital Deformities Associated with Monstrosities, and Incompatible 
WITH Extra-Uterine Life. 

1 For a general consideration of malformations of the central nervous sj'stem con- 
sult Tlioma, "Text-Book of Pathological Anatom}^" vol. i., p. 206 et seq. 

2 Van Gieson, "Artefacts of the Nervous Svstem," New York Medical Journal, vol 
Ivi., pp. 337, 365, 421, 1892. 



716 



THE NERVOUS SYSTEM. 



Tliese may be divided into : 

1. Amyelia, or absence of the spinal cord. Tliis is almost invariably associated 
with absence of the bi'ain. 

2. Aielomyelia, or partial development of the spinal cord. This is often seen in the 
anencephalous or acephalic monsters, where, corresponding to the incompletely developed 
brain, there may be various degrees of defective development in the length of the cord. 

3. Diastematomyelia, a condition in which a portion or the whole of the cord is 
split into two lateral halves. Each half of the cord, being enveloped in its own mem- 
branes and giving rise to its own nerve roots, may fuse together to form a single cord 
at some region. 

4. Biplomyelia, or a formation of two spinal cords — a duplication of the spinal cord. 
This happens in the various kinds of double monsters. 

II. Minor Congenital Malformations not Inconsistent with the Mainte- 
nance OF Life. 

1. HydrorrhacMs interna is a defective closure or arrangement of the divisions of the 
primary foetal central canal often resulting in the dilatation of the central canal by fluid 
{Hydromyelia) (Fig. 422). This dilatation may be moderate, or so extreme that but 
little of the substance of the cord is left as a thin shell around the central cavity. When 
they have not been destroyed by atrophy, epithelial cells may be found lining the cavity. 




Fig. 433,— Hydromyelia. 

In the section from which this drawing was made, the epithelial cells surrounding the dilated central canal 

were well preserved. 



This condition may be accidentally found after death. Its presence may also be 
indicated by its association with spina bifida. ^ 

2. Heterotopia, or misplacement of the substances of the cord. 
(«) There may be misplaced portions of the gray matter. 

{h) Portions of the white matter may be arranged in an unusual manner. 

3. Anomalies of the Spinal Nerve Roots. 

4. Asymmetries of the Spinal Cord. 

III. Malformations of the Spinal Cord Acquired during Extra-Uterine. 
Life or Secondary to Defective Development in Other Parts of the Body. 

1. Distortions following other cord lesions. 

2. Asymmetry of the cord due to arrested development after birth or to secondary 
atrophy of portions of the cord in association with defective development or absence of 
some other part of the body. 

_^ Under this subdivision the condition known as hydrorrhacliis externa may be con- 
veniently alluded to, which consists in an abnormal congenital accumulation of fluid 
between the meninges of the cord, causing more or less diminution in the volume of the 
latter. 



THE XEETOUS SYSTEM. 



17 



'<V1 



3. Asymmetry of the cord with congenital defects of the extremities or muscles, 
such as intra-uterine or other amputations, clubfoot, etc. 

4. Variations in the volume of the cord as a whole. 

False Heterotopia. — Congenital displacement of the gray or Avhite matter of the 
spinal cord — heterotopia — has been frequently described. Van G-ieson^ has shown, how- 
ever, that in a large proportion of cases the so-called heterotopia is an artefact (Fig. 
423) and has been caused by bruises or careless handling of the cord during its removal 
from the body or in the process of examination or hardening. 

Spina Bifida. — In the majority of cases hydrorrhachis is accompanied by a more or 
less complete lack of closure of the spinal canal posteriorly, so that the collections of 
Huid within may pouch outward through the 
opening in the form of a sac. The sac may 
be covered by skin, or this may be absent, 
either from the beginning or as a result of 
thinning and rupture. The walls of the sac 
may consist of the dura mater and the pia 
mater, or, in cases of hj^drorrhachis externa, 
of the dura mater alone ; when both are pres- 
ent they are usually more or less fused to- 
gether. Inside of the membranes of the sac 
there may be a shell of distended nerve tis- 
sue of the cord ; or the spinal cord may be 
split posteriorly and the sides crowded side- 
ways; or there may be a rudimentary frag- 
ment of the cord suspended in the sac or at- 
tached to the walls; or the cord may be but 
little changed and remain inside the spinal 
canal. The openings in the spinal canal may 
be due to the complete or partial absence of 
the vertebral arches, or more rarely the sac 

may protrude through openings between the completely formed arches. Spina bifida 
most frequently occurs in the lumbar and sacral regions, but it may occur in the dor- 
sal or cervical regions, or the canal may be open over its entire length. Very rarely 
it is open on the anterior surface. The protruding sac may be very small or as large 
as a child's head. The fluid in the sac is usually clear, but may be turbid from flocculi 
of de2:enerated nerve tissue. 




Fig. 423.— False Heterotopia. Section 
FROM Cervical Region of Spinal Cord. 

Showing: artificial displacemem of the struc- 
tures by an experimental bruise ("false hetero- 
topia ") after the removal of the cord from the 
body. (Van Gieson.) 



INJURIES OF THE BRAIN. 



The brain' may be directly Tvoiinded by a foreign body, or indirectly 
by fragments of bone driven into it, or it may be lacerated by severe 
contnsion withont fractnre or solntion of continnity of the sknll. It 
is very difficnlt to estimate the degree of injnry vrhich mnst canse 
death, since some persons die from slight, and others recover from very 
severe, wonnds of the brain. In incised wonnds of the brain more or 
less haemorrhage occurs at the seat of lesion, and the brain tissue in the 
vicinity soon undergoes degenerative changes. These may be compara- 
tiveh^ slight or extensive. Iniiammatory reaction may occur in the vi- 
cinity, and the adjacent brain tissue, as well as the haemorrhagic and de- 
generated area, may become infiltrated with pus cells. After a time the 
injured and degenerated area may become surrounded by new-formed 
connective tissue, and the decomposed extravasated blood and detritus 
1 Van Gieson, New York Medical Journal, vol. Ivi., pp. 337, 365, 421, 1892. 



718 THE NEEYOUS SYSTEM. 

of brain tissue, more or less fatty, may be absorbed, and thus after a 
time the part heals by a more or less i^igmented cicatrix. The healing is 
in most cases Yery slow and may occupy months or even years. The pia 
mater may participate to a marked degree in the inflammatory healing 
process. Abscesses may form near the seat of injury . 

After wounds which IuyoIyc the remoYal of i^ortions of the cranial 
bones, it is not uncommon after a few days to see a bleeding fungous 
mass project through the opening. This mass, sometimes wrongly called 
hernia cerebri, consists of degenerated brain tissue, blood, and granula- 
tion tissue, with more or less pus. The brain tissue below it is degener- 
ated, soft, broken down, and purulent, and there is often abscess in the 
adjacent brain tissue. Such wounds may fiually heal by the absorption 
of the broken-down brain tissue and blood, aud its substitution by gran- 
ulation tissue. 

Lacerations of the brain tissue without fracture may appear shortly 
after the injury as simj)le more or less circumscribed areas of capillary 
haemorrhage; the brain tissue about these may degenerate, pus may 
form, and abscesses be dcYcloped ; or the degenerated and lacerated tis- 
sue may be gradually replaced by granulation tissue which finally forms 
a cicatrix. The process of degeneration and softening and of healing 
in such lacerations of brain tissue may occur Yery slowly indeed, CYcn 
occupying years, and not infrequently the degeneratiYC changes are Yery 
extensiYe and progressiYC. In many cases, of course, the injury is so 
extensiYe, or IuyoIycs such important parts of the organ, that Yery little 
or no inflammatory or degeneratiYe change takes place before death. 

INJURIES OF THE CORD. 

The spinal cord may be compressed or lacerated by penetrating 
wounds, by fracture or dislocation of the Yertebrse, or by concussion 
without injury to the Ycrtebrge. The spinal cord is found simply disin- 
tegrated, or there may be much haemorrhage and the disintegrated nerve 
tissue be mixed with blood. If life continue, the nerve elements may 
degenerate ; Gluge's corpuscles and free fat droplets may form ; blood 
pigments may be formed ; and when inflammation supervenes more or 
less pus may be intermingled Ydth the degenerated material. There may 
be marked changes in the minute structure of the cord, without any 
change being evident to the naked eye. 

INJURIES TO NERVES. 

The secondary effects of injuries to nerves are described in the sec- 
tion on degenerations following injury. After amputation of a limb, 
there often occur swellings of the peripheral ends of the divided nerve 
trunks. These bulbous ends are called false or amputation neuromata. 
They are made up almost entirely of fibrous tissue, although nerve fibres 
have been found in them. 



THE NERVOUS SYSTEM. 



719 



HYPERTROPHY AND ATROPHY OF THE BRAIN. 

True Hypertrophy of the brain is rare, and probably always congeni- 
tal. An increase in the size of the brain from the proliferation of the 
neuroglia sometimes occurs in children either before or after birth, less 
frequently in youth, and very seldom in adults. The white substance of 
the hemispheres is increased in amount. If it take place before the ossi- 
fication of the cranium, the bones are separated at the sutures and fon- 




FiG. 424.— Atrophy of a CircuiMscribed Portion of Brain Convolutions in a Child. 
From a lesion of the corresponding blood-vessels. 



tanels; if after this, the inner table of the skull may be eroded and 
thinned. When the cranium is opened the dura mater appears tense and 
anaemic, the convolutions of the brain are flattened, the brain substance 
is firm and anaemic, the ventricles are small, the ganglia and cerebellum 
are either of normal size or compressed. 

The disease is usually very chronic, and destroys life with symptoms 
of compression of the brain. There may, however, be acute exacerba- 
tions. 

Atrophy. — This may occur as a senile change, or, in adults, in chronic 
alcohol, opium, or lead poisoning, in chronic insanity, and in chronic 
meningitis or from local interference with the circulation. In children 
who are much reduced by chronic diseases atrophy of the brain may ac- 
company atrophy of the rest of the body. 



720 THE NERVOUS SYSTEM. 

The atrophy affects principally the cerebral hemispheres, and may be 
uniform or more marked in some parts than in others, involving the 
whole of a hemisphere or of a lobe or only single convolutions or groups 
of these (Fig. 424). The convolutions are small, the sulci broad, the 
ventricles usually dilated, the brain tissue is firm, the gray matter discol- 
ored, the white substance grayish in color; the blood-vessels may be 
dilated. The basal ganglia may be small. Serum accumulates in the 
pia mater and in the ventricles ; the pia mater, and often the skull, be- 
come thickened ; the brain tissue may be oedematous or contain small 
haemorrhages. The nerve elements of the brain tissue are those most 
involved in the atrophy, the diminished areas being usually harder and 
firmer than normal. 



PIGMENTATION OF THE BRAIN. 

This may occur in any portion of the brain or its meninges from the 
decomposition of extravasated blood. In persons affected by malaria 
the gray matter of the brain has sometimes a dark or even blackish ap- 
pearance. This color is due to the presence of black pigment granules 
within the capillary blood-vessels. The obstruction to the vessels by 
masses of these x)igment granules may cause capillary apoplexies. The 
pigment may also be found in the walls and in the lumina of the vessels 
of the pia mater. 

Pigment patches of congenital origin are not infrequently seen in the 
pia mater. They may be due to the presence of branching pigmented 
cells. 



CUtCULATORY AND VASCULAR CHANGES IN THE BRAIN AND 

SPINAL CORD. 

Anatomical Considerations. 

In studying the circulatory changes in the brain and cord certain peculiarities in 
that circulation should be borne in mind. The vessels which nourish the brain arise 
from a remarkable anastomosis of large arterial trunks at its base, known as the circle 
of Willis (see diagram Fig. 425). From this " circle " pass off to each hemisphere three 
main branches — the anterior, the middle, and the posterior cerebral. These arteries 
ramify in the pia, where they anastomose freely. From this anastomosis small branches 
are given off which penetrate the brain substance, the shorter breaking up into capil- 
laries in the gray matter, the longer passing to the underlying white matter. After 
entering the cortex there is no further anastomosis, the capillaries of a cortical artery 
passing directly over into a venous system of capillaries without communicating with 
capillaries of other arteries. They are thus " terminal arteries." In addition to these 
arteries, which supply the hemispheres, branches from the circle of Willis are distrib- 
uted to the basal ganglia. These arteries are much larger than those which pass from 
the pia into the cortex, and beyond the circle of Willis do not form anastomoses with 
one another. Thus it is that occlusions of the arteries supplying the basal ganglia are 
much more serious, aside from the importance of the parts involved, \han of those pass- 
ing to the cortex. 

Three main arteries furnish blood to the cord: the anterior spinal, lying along. the 
opening of the anterior median hssure, and two posterior spinal, lying near the entrances 



THE NERYOUS SYSTEM. 



721 



of the posterior roots. Branches of these arteries anastomose in the pia, and from this 
pial network branches pass directly into the substance of the cord. The largest, a 
branch of the anterior spinal, passes into the pia of the anterior fissure, and penetrating 
the cord, is distributed to the gray matter of the anterior horn, and to the median gray 
matter as far back as Clarke's column. Smaller arteries from the posterior spinal supply 
the posterior regions of the cord. These arteries, like those in the brain, are terminal 
in the sense that, while anastomosing freely in the pia, after pene*'ating the substance 
of the cord there are no further anastomoses. 



Hyperemia and Anemia. 

The appearance of the brain tissue after death does not always fur- 
nish reliable indications of its blood contents during life, though it is 
perhaps more to be depended on than the ap- 
pearance of the meninges. 

Some of the more common conditions deter- 
mining Jiypeixemia which are mentioned aboYC as 
influencing the meninges apply also to the sub- 
stance of the brain. 

Active hypersemia may occur in various in- 
flammatory conditions of the brain. Hypersemia 
of the brain is quite common in deaths from in- 
solation and after conditions accomi^anied by 
acute delirium. Passive hypersemja may occur 
in conditions similar to those which determine 
congestions in other organs of the body, such as 
chronic diseases of the heart or lungs. It may 
be induced by anything which prevents venous 
return, such as intracranial tumors which com- 
press the sinuses, or by thrombosis. 

In sections of hyx)er8emic brains the small 
blood points from the cut ends of small vessels 
are more numeroiis and conspicuous than under 
normal conditions, and the brain tissue, i)artic- 
ularly the gray matter, jr^j have a diffuse red 
color. If excessive, the convolutions may be 
somewhat flattened, the brain tissue and pia 
mater may be oedematous, and the ventricles contain fluid, 
tion of the vessels may be general or localized. 

The most constant lesion of what is known as caisson disease, a con- 
dition resulting from exposure to sudden changes in atmospheric press- 
ure, is a congestion of the brain, cord, and meninges. Areas of soften- 
ing in the brain and cord are not infrequent and there may be effusion 
into the meninges. 

Ansemia of the brain may be either local or general. It may depend 

upon a general ansemia or upon general disturbances of the circulation, 

such as mitral stenosis or regurgitation ; or upon local interference with 

the arterial blood supply, such as complete or partial obstruction of the 

46 




Fig. 425.— Diagram of the 
Circle of Willis and Asso- 
ciated Vessels. 

a, Anterior cerebral; b, an- 
terior communicating ; c, inter- 
nal carotids; d, middle cere- 
bral ; e, posterior communicat- 
ing; /, posterior cerebral; g, 
basilar; h, vertebral. 



The conges- 



722 THE ISTEEYOUS SYSTEM. 

arteries from thrombi, emboli, inflammatory changes, spasmodic contrac- 
tions, etc., or from tumors, exudations, and blood extravasations press- 
ing upon the vessels from without. In oedema of the meninges, and in 
the presence of internal hydrocephalus, the brain tissue is apt to be 
anaemic. The brain tissue in anaemia looks whiter than usual, the con- 
trast between the gray and the white matter is less marked, and the 
small blood points usually seen on section from divided vessels may be 
very inconspicuous or almost entirely absent. 



CEdema. 

CEdema of the brain tissue may accompany either general or local- 
ized hypereemia, or it may accompany anaemia, and it seems in most cases, 
though not always, to be dependent upon conditions which induce these 
alterations in the blood contents of the brain. It is, perhaps, most com- 
mon in conditions which determine a passive hyperaemia. In some cases 
of marked impoverishment of the blood a so-called %^rcBmic oedema oi 
the brain is found. 

In oedema the brain tissue appears unusually wet and shiny. The 
same underlying condition is apt to determine an exudation into the 
membranes and ventricles. There is usually considerable distention of 
the perivascular lymph -spaces. 

Marked oedema of the brain may exist without brain symptoms. On 
the other hand, persons may die comatose with no other gross lesion than 
oedema, either with or without oedema of the pia mater. This is seen 
with especial frequency in acute and chronic alcohol poisoning, but may 
occur under other conditions. A careful microscopical examination of 
the brain under these conditions will frequently reveal structural lesions 
of more serious import than the oedema. 

Under the designation of '^serous apoplexy," oedema of the brain was 
formerly considered of importance, in the absence of other lesions, as a 
cause of death. But increased knowledge has led to the general belief 
that simple cerebral oedema as an independent condition has not the sig- 
nificance formerly ascribed to it, and it should be accepted, if ever, with 
great reserve as a cause of death. 



H^MOEEHAGE. 

Haemorrhages in the substance of the brain may be very small and punc- 
tate, and are then usually called cainUary hcemorrliages ; or they may re- 
sult in the collection in the brain tissue of masses of blood of consider- 
able size, which are called apoplectic foci or clots. These forms of 
haemorrhages may be associated, or a number of capillary haemorrhages 
may join to form an extensive clot. 

Capillary hwmorrhages may appear, on section of the brain, like the 
severed ends of hyperaemic blood-vessels, or the tissue about them may 



THE NERVOUS SYSTEM. 723 

be more or less tinged with blood. Microscopically, tlie perivascular 
spaces are distended with blood, which may have escaped into them; 
fchis is associated with more or less broken-down brain tissue. The haem- 
orrhages may be single, but are frequently multiple, so that the brain 
tissue is besprinkled with blood points. Degeneration of the extrava- 
sated blood may give rise in later stages to reddish or brown or yellowish 
circumscribed discoloration of the brain tissue, due to granules and crys- 
tals of blood pigment intermingled with broken-down brain tissue, with 
more or less fatty degeneration of its elements. Capillary haemorrhages 
may be due to fatty degeneration of the vessels leading to rupture ; or 
the extravasation may be due to diapedesis, or it may depend upon con- 
ditions which we do not understand. They frequently occur in the 
vicinity of apoplectic clots and tumors, they may be due to thrombosis 
of the veins or of the sinuses of the dura mater ; they not infrequently 
occur in acute encephalitis, in congestive hypersemia, in acute mania, 
and in delirium tremens ; and they may be associated with general dis- 
eases, such as scurvy, purpura hsemorrhagica, typhus fever, pyaemia, 
ulcerative endocarditis, etc. ; they may be associated with embolic soft- 
ening. 

Apo])lectic foci may result from the coalescence of numerous capillary 
haemorrhages; from injury, or from mixture of diseased arteries, either 
with or without changes in the blood pressure. Haemorrhages from in- 
jury to the skull may occur as well without as with fracture, and may be 
situated over the vertex as well as at the base of the brain, and vary in 
extent and seat, dependiug upon the character and point of the injury 
and the size of the vessels involved. The so-called spontaneous haemor- 
rhages, other than those of capillary origin, which give rise to masses of 
blood and broken-down brain tissue, may vary in size from that of a pea 
to those occupying a large part of a hemisphere. They are due, in a 
very considerable proportion of cases, to the rupture of small arterial 
aneurisms, but may arise from weakening of the walls of the arteries, 
from arteritis, atheroma, or fatty degeneration. These latter forms of 
lesions doubtless give rise in most cases to the formation of the aneurisms 
whose rupture is in so many cases the immediate cause of the haemor- 
rhage. 

Aneurisms of the cerebral arteries may be as large as a pea or 
hazelnut, but those most frequently met with and causing apoplexy are 
usually small— called miliary aneurisms — and may be microscopic in 
size, varying from this up to that of a large pin's head or larger. They 
may be sacculate or fusiform, and frequently exist in considerable num- 
bers. They may occur in any of the small arteries of the brain, but are 
said to be most frequent on the branches of the middle cerebral artery. 
It is asserted that the bursting of miliary aneurisms is the nearly if not 
quite exclusive cause of the formation of spontaneous apoplectic clots, 
but this we do not believe to be true. 

As to the immediate cause of rupture, either of aneurisms or other- 
wise diseased blood-vessels in the brain, we are in many cases entirely 



724 THE NERVOUS SYSTEM. 

ignorant. In some cases it seems to be due to an increased arterial ten- 
sion in such diseases of the heart as induce this change, as in the car- 
diac hypertrophy which may accompany some forms of chronic diffuse 
nephritis ; or it may result from unusual exertion or mental excitement. 

The most frequent seat of hsemorrhage is in the corpora striata and 
optic thalami (Fig. 426), and the brain tissue in their vicinity, and here 
they occur most often in the parts supplied by the branches of the mid- 
dle cerebral artery. The possibility of haemorrhage in the floor of the 
fourth ventricle should be borne in mind in investigating cases of sud- 
den death from obscure causes. 

Hsemorrhages frequently seriously affect other portions of the brain 
than those immediately supplied by the ruptured vessels. Thus haemor- 
rhages in the cortical substance or beneath the pia mater may force their 
way deep into the brain substance ; or, in haemorrhage in the brain sub- 
stance, the blood may burst into the ventricles or work its way into the 
intermeningeal space, and, either at the seat of its occurrence or in the 
situations into which it is forced, may give rise to serious compression 
of the brain. Portions of the brain containing large extravasations may 
be enlarged, the tissue anaemic from pressure, the convolutions flattened, 
and the surface dry. As the blood is poured out, the brain tissue is usu- 
ally torn and lacerated, so that the apo]3lectic clot usually consists of 
detritus of brain tissue intermingled with blood. If, however, the blood 
is poured out from a single vessel, the lacerated brain tissue may be 
pressed aside, and the greater portion of the red mass may consist of 
pure blood clot. 

The appearances presented by haemorrhages in the brain vary greatly, 
depending u^Don the time which has elapsed since their occurrence. If 
life continue, the oedema which usually soon occurs in the vicinity of the 
haemorrhage disappears and the clot becomes drier and firmer ; gradually 
the blood undergoes the usual series of changes seen in extravasation ; 
the haemoglobin decomposes, forming granules and crystals of blood pig- 
ment ; the blood cells and fibrin undergo degeneration and absorption ; 
the detritus of brain tissue undergoes fatty degeneration. As these al- 
terations occur the color changes to reddish-brown, orange, or yellow, 
and the adjacent brain tissue may be discolored by imbibition. 

Inflammatory reaction may occur in the vicinity, leading either to the 
formation of a more or less pigmented cicatrix, or to a cj^st with yellow- 
ish fluid contents and a fibrous, more or less pigmented wall. The proc- 
ess of degeneration and absorption of the blood and broken-down brain 
tissue, and their replacement by a cyst or by a cicatrix, is a slow one, 
and the cysts and cicatrices may resemble those formed at the seat of 
embolic softening. Kot infrequently we find in the brain of a person 
dead from recent apoplexy the remains of old clots presenting some one 
of the above -described stages of absorption. The apoplectic cysts and 
cicatrices persist for a long time after their formation. 

Secondary degenerations (see page 741) following haemorrhages de- 
pend entirely upon the cells destroyed or the fibre tracts interrupted. 



THE XEEYOUS SYSTEM. 



'25 



Most common are degenerations of the pyramidal tracts from lisemor- 
rliages into the sensory-motor region of the cortex, or from hfemorrhages 
into the internal capsnle (lenticulo-striate arterj^). Haemorrhages in- 
volving the optic centres or the optic fibres lead to degeneration in the 
optic tracts. Haemorrhages into other portions of the brain, by destroy- 




S 4-1 

•'- o 
CO !5£ 

■" a 

81 






S :ll 

S ^3 



1^ 



cS 3 






ing commissural cells or interrupting their fibres, lead to degeneration of 
intracranial fibre tracts. 

Haemorrhage in the Spinal Cord is much less frequent than in the brain, 
but may occur either as capillary apoplexy or as larger apoplectic clots. 
Capillary haemorrhages, similar in appearance to those of the brain, may 
occur as the result of injury, or near areas of softening or tumors, or may 
accompany severe convulsions, as in tetanus. Apoplectic clots, which 
are comi)aratively rare in the spinal cord, are usually small, commonly 



726 THE I^TERVOUS SYSTEM. 

not more tlian 1 cm. in diameter, and are similar in their appearance, 
and in the changes subsequent to their formation, to those in the brain. 
They are usually the result of injury; but may occur spontaneously. 
These so-called ^^spontaneous haemorrhages^' are undoubtedly in most 
cases the result of inflammation. They may occur in any acute disease 
of the cord, and are an especially frequent complication of acute myelitis. 
Hcemorrhage into the cord, occurring in the course of an acute infectious 
disease, is probably, as a rule, due to an unrecognized myelitis or acute 
degeneration. Hsemorrhages in the course of a chronic myelitis are not 
common, and are probably due to a softening dependent on interference 
with nutrition. Haemorrhages into the cord have been reported in syphi- 
litic myelitis, in syringomyelia, and in tumors of the cord. Gliomata 
especially are often very vascular, and their thin-walled vessels are sub- 
ject, to rupture. Sometimes, however, haemorrhagic foci are found in 
the spinal cord without traumatism or evidence of inflammatory change. 
Larger haemorrhages naturally follow the lines of least resistance, and 
their long diameter corresponds to that of the cord. To such columnar 
haemorrhages, usually traumatic in origin, the name hccmatomyelia has 










^S 



Fig. 427.— Section of the Spinal Cord Showing Hemorrhage into the Gray Matter and Ex- 
tending Lengthwise of the Cord. (An early pbase of haematomyelopore.) 

This lesion is sometimes called " haematomyelia." 



been applied (Fig. 427). The term is being now more properly used to 
cover the general subject of haemorrhage into the spinal cord. 

The smaller capillary haemorrhages may be entirely absorbed. They 
may, on the other hand, form microscopic sclerotic areas. The larger 
haemorrhages determine a considerable destruction of tissue. They may 
be absorbed and replaced by fibrous tissue, or the central area may break 
down into a fluid or semi-fluid mass of blood and tissue, with a more or 
less definite fibrous wall (Fig. 428). To these columnar cavities or canals 



THE NERVOUS SYSTEM. 727 

the term Jicematomyelopore has been applied by Yan Gieson. ^ To a simi 
lar conclitiou in which proliferation of the neuroglia is the most marked 
feature, the name of '4"alse or secondary syringomyelia^' has been given. 



Thrombosis and Embolism. 

Thrombi may form in the arteries as a result of any degenerative or 
inflammatory x)rocess in their walls leading to a roughening or death of 
the intima, or from pressure from without, or they may occur in vessels 









.i^_^-'^ 



Fig. 428.— H^matomyelopore. 



The section shows at one point a cyst-like cavity in the spinal cord, originating in a hgemorrhage in the 
posterior root (see Fig. 427) and extending nearly the entire length of the cord. The cavity is lined hy tis- 
sue detritus and neuroglia. 

in whose walls we can detect no primary lesion. The most common 
causes are atheroma and simple endarteritis. Thrombi may also form 
around an embolus which does not entirely occlude the vessel. 

Emboli of the cerebral arteries most commonly arise from acute or 
chronic endocarditis or cardiac thrombi ; they may arise from aneurisms 
or atheroma of the aorta, from the carotid or vertebral arteries, or from 
the pulmonary veins. The materials constituting emboli vary greatly, 
depending on their mode of origin (see page 75). The effects on the 
brain tissue of emboli and thrombi of the arteries are essentially the same 
in their main features. In some cases, however, in which large emboli, 
usually from endocarditis, suddenly block up a large vessel, the individ- 
ual may die almost instantly without other apparent lesion than the stop- 
page of the vessel. 

""Yan Gieson, " Haematomyelopore — a New Spinal-Cord Disease." New York Poly- 
clinic, 1897, vol. X., p. 87. 



728 



THE XEEVOUS SYSTEM. 



In general, the first effect of the occlusion of an artery is to deprive 
the region to which it is distributed of blood. In arteries whose branches 
anastomose, the affected area is soon suxDplied with blood by the estab- 
lishment of a collateral circulation. In terminal arteries, on the other 
hand, the blocking of the vessel is followed, as a rule, by degenerati^ e 
changes and softening in the brain tissue. The appearances which these 
degenerated areas present vary greatly, depending upon the stage of the 
degeneration and the amount of blood which may be extra vasated. Dense 




Fig. 439.— Degenerated Cells, Cholesterin Crystals, and Corpora Amylacea from Brain Tis- 
sue IN Embolic Softening. 

a. Fatty ganglion cells ; &, corpora amylacea ; c, cell containing very large number of fat droplets (com- 
pound granular or Gluge's corpuscles) ; d, cholesterin crystals. 



infiltrations of the brain tissue with blood, as in hgemorrhagic infarctions 
from emboli in other parts of the body, do not usually occur, although 
considerable blood may be extravasated. Areas of softening in which 
there is little extravasation of blood are usually white or yellow in color, 
white or yellow softening. When much blood is present the process is 
frequently called red softening. Yellow softening is probably often only 
a secondary stage of the red, resulting from absorption of most of the 
pigmeiit. The term ^^ white softening ^^ is often used interchangeably 
with ^' yellow.^' It is also applied to that condition into which the latter 
passes after more complete liquefaction, and after fatty changes have 
taken place. Young proliferating neuroglia tissue often gives a glisten- 
ing white appearance to the lesion. 

The tissue in the affected area gradually softens and may become dif- 
fluent. Microscopically, the softened tissue is seen to consist of more or 
less fluid with broken-down brain tissue, fragments of nerve fibres, drop- 



THE NERVOUS SYSTEM. 



729 



lets of myelin, nerve cells, shreds of neuroglia tissue and blood-vessels, 
and red and white blood cells. The evidence of degeneration is seen 
in the presence of fat granules and droplets, larger and smaller cells 
densely crowded with droplets of fat (so-called Gluge's corpuscles or com- 
pound granuJar corpuscles). Various kinds of cells and cell fragments, 
more or less granular and fatty, and also corpora amylacea, blood i^ig- 
ment, fat crystals, and cholesterin crystals, may be found (Fig. 429). 
The walls of the blood-vessels may also be in a condition of fatty degen- 
eration (Fig. 430). The color of the softened mass will of course depend 
upon the relative amounts of these elements. 

The tissue may remain for a long time in the soft condition, or it 
may be absorbed and replaced by a connective -tissue cicatrix which 
may be more or less pigmented; or a wall of connective tissue may 
form about it, converting it into a well-defined cyst, with or without 
pigmented walls ; or the mass may dry and form a dense, structureless 
nodule. Acute inflammatory changes may occur about the dead tissue. 
In cases of infectious emboli numerous abscesses may be formed in addi- 
tion to their mechanical action. 

Thrombi are most frequent in the internal carotids, less so in the 
middle cerebral, basilar, and vertebrals. They may occur, but still less 
frequently, in other cerebral arteries. Emboli are most common in the 
middle cerebral artery, next in the internal carotid, and then in the basi- 




FiG. 430.— Blood-Vessels from an Area of Embolic Softening of Brain. 
The walls of the vessels, particularly the endothelial cells, contain fat granules and fat droplets. 



lar. The relative frequency with which embolism occurs in the middle 
cerebral artery is attributable to the directness with which the blood 
passes into this artery from the heart. The great significance attaching 
to embolism of the middle cerebral artery is evident when we remember 
that its branches within the brain are terminal arteries, and are dis- 
tributed to such important structures as the lenticular and caudate nuclei, 
the internal capsule, and the optic thalamus. 

Thrombosis and embolism also occur in the vessels of the spinal cord, 
though less frequently than in those of the brain. As in the brain, when 



730 THE NERVOUS SYSTEM. 

they involve terminal arteries, they determine areas of softening and 
consequent secondary degenerations. 



Lesions of the Vessel Walls in the Brain and Cord. 

The mural changes in the vessels are not peculiar to the nervous sys- 
tem: the most frequent is that known as atheroma or arterio- sclerosis. 
It is especially common in the system of arterial trunks which make up 
the circle of Willis. Fatty degeneration is often found in the vessel 
walls coincident with the increase in the connective -tissue elements. 
Calcification may occur and may be so extensive that the whole or a 
greater part of the circle of Willis is converted into a series of hard 
tubes usually somewhat larger than normal. More commonly the cal- 
careous areas are irregular in their distribution, giving to the vessels a 
nodular appearance. Fatty degeneration may also occur, though more 
rarely, as an independent lesion. It affects particularly the muscular 
coat. Hyaline degeneration may also occur either as an independent 
lesion, which is quite frequent in the brains of idiots, or as the initial 
lesion of a sclerosis. 



DEGENERATION AND INFLAMMATION IN THE BRAIN, SPINAL 

CORD, AND NERVES. 

Review of Normal Morphology. 

While the scope of this work does not warrant a detailed description of the mor- 
phology of the nervous system,^ our conception of its ultimate structure has recently 
been so completely revolutionized and our appreciation of the pathological changes to 
which it is subject is so dependent upon an accurate knowledge of its morphology, that, 
before proceeding further a brief resume of some of the more fundamental points in 
its structure and architecture cannot wisely be omitted. 

The long accepted belief in a diffuse and anastomosing nerve network has now been 
supplanted, and the studies of Golgi and of his successors in the use of his technique 
have placed upon a firm basis the so-called neurone conception of nervous-sj^stem 
structure According to this view, the neurone represents the structural unit of the 
nervous system. The neurone is the nerve cell with all its prolongations, and the ner- 
vous system in toto is but an orderly association of an immense number of these neurone 
units. Although these neurones differ from one another as to details of structure they 
still present an essential similarity. 

The neurone is first distinguishable as a small round cell in the epiblastic lining of 
the embryonic neural canal. Such a cell is entirely devoid of processes. It soon, 
however, becomes pyriform, and from the tip of the pear grows out a process, which is 
the axis-cylinder process or axone. Later other processes appear as outgrowths of the 
cell body. These are the protoplasmic processes or dendrites. Each adult neurone 
then consists of a cell body, and passing off from this cell body two kinds of processes 
Figs. 431 and 432). 

The Cell Body. — Our knowledge of the internal structure of the nerve cell has been 
greatly increased in the last few years by the application of a special technique devised 

^ For this the reader is referred to such works as " The Nervous System, " by 
Barker, and the "Anatomic du Systeme Nerveux de I'Hemme," by Van OeTiiichten. 



THE NEEYOUS SYSTEM. 



731 



by Nissl.i Subjected to this technique nerve cells present two very different types of 
reaction. Certain cells, such, for example, as the cells of the granule layers of the cere- 
bellum and of the olfactory lobe, stain only as to their nuclei, the cell bodies themselves 
remaining entirely unstained. To such cells Nissl has given the name of caryocliromes. 
It is obvious that the method of Nissl gives no insight into the structure of these cells. 
The majority of nerve cells, however, react both 
as to their nuclei and as to their cell bodies to 
the Nissl stain. These cells Nissl designates as 
somatochromes. Such a cell presents the follow- 
ing appearance (Plate XIII., 1). There is a nu- 
cleus identical in structure with nuclei found in 
other cells. It is bounded by a nuclear mem- 
brane and traversed by a network which takes a 
comparatively light blue stain. AYithin the nu- 
cleus is a nucleolus staining an intense blue. 
In the cell body two distinct elements appear : 
a clear ground substance, unstained; and scat- 
tered through it deep blue staining masses, 
known as chromophilic hoclies. These cliromo- 
pliilic bodies are granular, and differ in size, 
shape, and arrangement. These differences 
have served as a basis of classiiication. Pre- 
senting variations in different types of cells, 
their appearance in a given type remains con- 
stant. Most investigators, while differing in 
details, agree in ascribing to the unstainable 
substance a definite structure. This structure 
is usually described as composed of a fibrillar or 
reticular netAvork lying in a more or less homo- 
geneous ground substance. With the use of the 
ordinary technique of Nissl, all of the cell body, 
excepting the chromophilic bodies, remains un- 
stained and apparently structureless. Our ideas 
as to the physiology of these different elements 
of the nerve cell rest largely upon a theoretical 
basis. It has been shown that the nerve cell 
represents the genetic centre of the neurone. 
From the behavior of the processes, when cut 
off from the nerve cell, it is evident that the cell 
body represents the nutritive or trophic centra 
of the neurone. It seems probable that from the 
standpoint of neurone activity, the cell body re- 
presents the functional centre of the neurone, 
while the processes act as organs of reception or 
of distribution. Certain facts, such as the entire 
absence of the chromatic substance in many 
nerve cells, in the axones of all nerve cells, and 
its diminution during functional activity and in 
fatigue, together with its behavior under certain 

pathological conditions, lend weight to the view that the stainable substance of Nissl 
represents a food element of the cell. The achromatic element, on the other hand, is 
continuous with the fibrillae of the axone, and is considered by most investigators as repre- 
senting the essential nervous mechanism of the cell. The relation of the Nissl picture 
to the conditions existing in the protoplasm of the living cell still remains an unsolved 
problem. The importance of the Nissl method from the standpoint of pathology lies 




Fig. 431.— Neurone (Nerve Cell or 
Ganglion Cell and Processes) from 
Human Cerebral Cortex. 

Showing main or apical dendrite passing 
upward and numerous smaller dendrites 
coming off from the main dendrite and from 
the hody of the cell. A single axone (axis- 
cylinder process) passes downward from the 
base of the cell, giving off two collaterals. 



^ See Nissl's method of staining, p. 770. 




732 THE NEEYOUS SYSTEM. 

in the fact that when subjected to a given technique, a given type of nerve cell presents 
always the same appearance, and that this appearance furnishes a norm for comparison 

with cells showing pathological changes and 
which have been subjected to the same technique. 
Pigment. — In addition to the elements already 
described, more or less pigment in the shape of 
fine greenish-yellow granules (Xissl technique) is 
often present in nerve cells. It is not found in 
cells of the new-born. It increases with age, and 
in old age often fills up a large part of the cell 
body. Its significance is not known. 

The protoplasmic processes or dendrites are — at 
least the larger trunks — of the same structure as 
the cell body (Plate XIII., 1). That these larger 
trunks have functions similar to those of the cell 
body seems probable from the fact that the axone 
not infrequently takes origin from a large dendri- 

FIG. 433.-NEURONE (NERVE CELL OR ^^^ ^^'^f ^ ^^^^"^^^ ^^ ^"'^^^^^^ ^^'^^^ ^^^ ^^^^^ ^^ 

Ganglion-Cell PROCESSES). From the tlie cell. The chromatic substance is present in 
Granular Layer of the Cerebellar the dendrites, as elongated rods with triangular 
Cortex of a Guinea-Pig. masses at the points of bifurcation. The achro- 

Tbe short axone passes off to the left and matic elements are apparently of the same charac- 

terminates near its cell of origin. ter as in the body of the cell. The protoplasmic 

processes divide dichotomously, becoming rapidly 
smaller, and end at a comparatively short distance from the cell body.^ Stained by the 
method of Golgi, the dendrites are seen to be covered with minute projections or 
"gemmules," often ending in a small bulb. These processes are cellulipetal in charac- 
ter, carrying impulses always toward the cell. 

The axis-cylinder pirocess or axone — so-called from its often becoming the axis cylin- 
der of a nerve fibre — is usually single. It generally arises directly from the body of the 
cell, but may arise, as already mentioned, from one of the larger protoplasmic trunks. 
It is differentiated from the dendrites in Nissl preparations b}^ always taking origin 
from an area in the cell body free from chromatic substance, and by being itself entirely 
achromatic (Plate XIII., 1); in Golgi specimens, it is recognized by its straight course, 
uniform diameter, and smooth outline (Fig. 431). It sends off few branches, and these 
at right angles (collaterals). This axone may extend a great distance from the cell 
body ; for example, the axones of certain motor cells of the spinal cord extend to tlie 
muscles of the hands or feet. Both the axone proper and its collaterals end in terminal 
arborizations. Their conductivit}^ is cellulifugal — that is, they always carry impulses 
from the cell. In certain cells the axis-cylinder processes branch rapidly and end in 
the gray matter in the vicinity of their cells of origin (Fig. 432). An axone may pass 
from its cell of origin to its termination uncovered by any sheath. Such axones are 
found in certain portions of the graj^ matter. An axone may be enveloped only by a 
thin membrane, the sheath of Schwann, as, e.g. , the fibres of Remak found mainly in 
the sympathetic system. An axone may be surrounded by a myelin sheath alone, as 
in the white matter of the brain and cord, or by both a myelin sheath and a sheath of 
Schwann, as in the fibres of the peripheral nerves, with the exception of the olfactory 
and optic. 

Each neurone represents a morphological, and to a certain extent a physiological 
entit3^ Association between neurones is believed by most investigators to take place 
by contact or contiguity and not by continuity of their protoplasm.- The passage of 

1 Exception, periplieral arm of spinal ganglion cell. 

'-^ The validity of the neurone doctrine has been recently called in question by such 
investigators as Held, Apathy, Bethe, and Xissl. For a critical review of the opinions 
of these writers, consult the last edition of Van Gelmchten's " Anatomic du Systeme 
Nerveux." 



THE NEEYOUS SYSTEM. 



733 



an impulse is probably always from the axonal arborizations of one neurone to the 
dendrites or cell body of another neurone. 

The cell bodies of neurones are grouped mainly in the gray matter of the brain and 
cord, in the ganglia of cranial, spinal, and sympathetic nerves, and in the peripheral 
end organs of (;ertain of the nerves of special sense. Protoplasmic processes ramify 
mainly within the gray matter. ^ While some terminate in the gray matter in the imme- 
diate vicinity of their cells of origin, it is the axones that make up the bulk of the white 
matter of the brain, cord, and peripheral nerves. 

Neuroglia. — In addition to the extensions inward of the pia mater and the connec- 
tive tissue of the blood-vessels, there is found in both gray and white matter a tissue, 
probably supportive in function, and peculiar to the nervous system — the neuroglia. 
Like the neurone, it originates in the epiblastic cells lining the embryonic neural canal. 
These cells, at first morphologically identical, soon differentiate into neuroblasts, or 
future neurones, and spongioblasts, or future neuroglia cells. In the adult two main 
types of neuroglia cells are found, spider cells (Fig. 433), with spine-like, straight, 
unbranching processes, and mossy (Fig. 434) cells with thick, rough, branching arms. 
The former are found chiefly in the white matter, the latter in the gray matter in con- 
nection with blood-vessels. As in the case of the nerve cell, the processes of these cells 
do not anastomose, but interlace, forming a dense feltwork. By a special stain, Y^ei- 
gert demonstrates neuroglia cell nuclei and separate fibrils. It seems probable that 
this method fails to show the body of the cell, while staining its nuclei and the fibrils 
which pass through it. 

It would thus appear that the architecture of the central nervous system, consid- 
ered as an organ, is analogous to that of other organs. It has in the neurone its paren- 
chyma, and this parenchyma is supported and bound together by a framework of con- 
nective tissue. The essential difference lies in the fact that in the neurone is the highest 





Fig. 433.— Neuroglia Cell— Spider 
Type— HrMAX Cerebrum. 



Fig. 434. 



-Neuroglia Cell— mossy Type- 
Human Cerebrum. 



morphological difl'ereutiation which protoplasm has attained, and representing chem- 
ically the most complex molecules known. In the axone, sometimes a metre or more 
in length, of a cell o-f microscopic dimensions, there is a distribution of cell protoplasm, 
such as occurs in no other tissLie or organ. The neuroglia also, while without question 
a tissue supportive in function, is embryologically and morphologically different from 
other forms of connective tissue. 



Exception, peripheral arm of spinal ganglion cell. 



Explanation of Plate XIII.' 

1. Normal Ganglion Cell. Sticliocbrome from anterior horn of liumaii spinal cord, 
showing the nucleus in its normal central position with its nucleolus. In the body 
of the cell are seen the chromophilic bodies of various shapes and sizes. Three 
main protoplasmic trunks or dendrites pass oft: from the upper portion of the cell. 
In these the chromophilic bodies are rod-shaped. The largest process branches at 
a short distance from the cell. To the left is seen the axone or axis-cylinder pro- 
cess free from chromatic substance, as is also that portion of the cell from which it 
takes origin (axone hill). 

3. Ganglion Cell from the Anterior Horn of the Human Spinal Cord op a 
Case of xAlcoholic Neuritis. Showing eccentricity of the nucleus and a large 
central area of the cell body free from chromatic substance (central chromatolysis), 
with an arrangement of the remaining chromophilic bodies around the peripliery. 
(The similarity between the appearance of this cell and the one shown in Fig. 6 
should be noted.) 

3. Ganglion Cell from the Anterior Horn of the Spinal Cord of a Rabbit 

Inoculated with Rabic Virus and Killed Shortly After the Onset of 
Symptoms. Shows an early stage of chromatolysis ; the chromophilic bodies being 
pale, ragged, and vacuolated. 

4. Ganglion Cell from the Anterior Horn of the Spinal Cord of a Rabbit 

w^HiCH Died on the Ninth Day After Inoculation with Rabic Virus. 
Shows extreme chromatolysis, only a few fine granules of chromatic substance re- 
maining at the periphery. The cell is swollen, the nucleus has disappeared, and 
the cell bod}" and processes are stained more deeply with the erythrosin than is the 
case in normal cells. 

5. Normal Ganglion Cell from a Human Spinal Ganglion of the Posterior 

Root. Showing central position of the nucleus and the concentric arrangement of 
the chromophilic bodies. 

6. Ganglion Cell from the Posterior Root Ganglion of a Rabbit Three 

Weeks After Section of the Sciatic Nerve. The cell shows extreme eccen- 
tricity of the nucleus with central chromatolysis and a peripheral arrangement of 
the remaining chromophilic bodies^axonal degeneration. (There also remains in 
the central portion of the cell some chromatic substance in the shape of fine granules 
forming an irregular reticulum. The similarity between this picture and the one 
shown in Fig. 2 is apparent.) 

7. Portion of a Posterior Root Ganglion from a Case of Tabes Dorsalis. 

Showing degeneration in the ganglion cells with increase in the interstitial connec- 
tive tissue. 

8. Two Pyramidal Cells from the Normal Human Cerebral Cortex. While 

the pyramidal cells in the human cortex vary considerably in the amount of chro- 
matic substance which thej contain, these are of an average type. 

9. Two Pyramidal Cells of the Human Cerebral Cortex from a Case of 

Eclampsia. These cells show marked chromatolysis. 

1 In the staining of the specimens from which these drawings were made, Held's modiflcation of 
Nissl's method was used. This consists essentially in a preliminary staining of the sections with a one-per- 
cent aqueous solution of erythrosin (see p. 770) . 



Pathology — Delafield & Prudden. 



Plate Xill. 



xV 









,.;i-^T' 



FIG 5. 



N 



FlQ. 2. 



FIG 3. 



I 



%;■ 






,..^^'^iv^ o 



S.*^^; 



FIG. 6. 



- » . ' 



V-* 



Lesions of Ganglion Cells. — (Stained by Nissl's Method. 

Drawn by F. R. Bailey. 



THE NEEYOUS SYSTEM. 



'35 



DEGENERATION. 



Neurone Degeneration. 




Fig. 435. -Neurone Degenera- 
tion After Injury. 

Teased nerve fibres from distal 
portion of sciatic nerve of rabbit 
three weeks after division of the 
nerve. Osmic-acid stain. The large 
and small black masses represent 
disintegrated myelin and fat drop- 
lets. 



DegeneratiYe changes may affect the entire neurone or any of its 
parts. Such changes may result from direct injury to some part of the 
neurone, to diminution or modification of its nutritiYe supply, to various 
toxic conditions, etc. 

I. Changes in the Neurone from Injury to One of its Parts.— («) Changes 

IN THE AXONE EESULTING FROM SEPARATION FROM ITS CeLL BODY. 

— That changes, presumably of a degenera- 
tive character, occur in the peripheral end 
of a nerve when its connection with the cen- 
tral nervous system is broken has long been 
known. This degeneration takes place as well 
in the central as in the perij)heral nervous 
system, and is complete, involving every por- 
tion of the axone distal to the point of section. 
The changes are not progressive from the 
X)oint of lesion, but occur at nearly the same 
time in all parts of the distal stumj). These 
changes consist in a breaking up of the 
medullary sheath into segments (Fig. 435), 

which in turn disintegrate, forming variously shaped masses of myelin, 
among which may be seen the axis cylinder, the whole being enclosed by 
the neurilemma. The method of Marchi (see page 769), which differen- 
tiates between fat and myelin, shows that coincident with the breaking 
up of the myelin there is an appearance of fat droplets (Fig. 436). These 
fat droplets increase in number pari passu with the decrease in myelin, 
but also ultimately disappear. During the progress of these changes in 

the medullary sheath, the axis cylinder at first 
segments and then undergoes dissolution. The 
neurilemma, on the other hand, appears to 
take no part in the degenerative process. On 
the contrary, it and its nuclei remain intact to 
take part later in regenerative changes, should 
these occur. If there is no reunion of the sev- 
ered ends of the axone, the peripheral portion 
completely disappears, its place being taken 
by connective tissue. 

(h) Changes in Dendrites Eesulting 

FROM THEIR SEPARATION FROM THEIR CeLL 

Bodies. — If we consider, as does Van Gehuch- 
ten, ' that the peripheral arm of the spinal ganglion cell is a protoplasmic 
process, making a physiological rather than a morphological differentia- 
tion, we find that the same law holds good for dendrites as for axones 

^ Van Gehucliten, " Anatomic du Systeme Nerveux de rHomme," p. 313. 



:3?rf:ii» 



Fig. 436.— Neurone Degenera- 
tion After Injury. 

Longitudinal section of distnl 
portion of the same nerve. Mar- 
chi staiu. The black dots repre- 
sent droplets of fat resulting from 
degeneration of the medullary 
sheaths. 



736 THE NERVOUS SYSTEM. 

when separated from their cell bodies. Thus in the divided peripheral 
nerve those fibres which are the processes of the spinal ganglion cells 
present the same degenerative changes as do the fibres which are proc- 
esses of cells of the anterior horn. Most dendritic processes are, how- 
ever, so short and terminate in the gray matter so near the cells from 
which they originate that experimental separation of the process from 
its cell body is impracticable. In view of the fate of the axone, however, 
and the relation of the dendrites to the cell body, there can be little 
doubt that as complete degeneration follows the severance of a proto- 
plasmic process from its cell of origin as follows in the case of the axone. 

(c) Changes in the Proximal Stump and in the Cell Body 
Eesulting from Lesion to the Axone. — The fundamental principle 
of the law of Waller was the complete degeneration of the distal portion 
of the divided nerve, while the proximal stump remained intact. Our 
present conceptions, however, of the interdependence of the different 
parts of the neurone, and of the axone as the outlet for neurone energy, 
would lead us to expect certain changes of an atrophic nature in the 
proximal stump aoid in the cell body, as a result of separation from its 
axone and consequent inability to functionate. That such changes take 
place recent improvements in cytological technique have enabled us 
to determine. The method of Marchi shows that degenerative changes 
occur not only in the distal, but in the proximal end of the divided 
nerve. These changes take place more slowly than in the distal portion 
but are apparently identical in character. 

In the body of the cell the method of Nissl demonstrates marked 
changes after section of the axone. These changes may be observed 
within twenty -four hours after the injury. They consist in a diminu- 
tion in the chromatic elements of the cell, chromatolysis. This is most 
marked in the central portion (central chromatolysis), a distinct ring 
of chromophilic bodies around the periphery often remaining. The 
nucleus usually migrates toward the periphery and may even bulge 
from the cell. In the case of the hypoglossal nerve in the rabbit, these 
changes reach their maximum in from two to three weeks. The future 
of some of these cells is complete degeneration. Others apparently un- 
dergo regeneration. The intensity of the reaction of the nerve cell to 
injury to its axone depends upon the severity of the injury. Thus cut- 
ting the nerve is followed by more prompt and marked changes in the 
nerve cell than simple compression, while pulling out the nerve roots is 
followed by a still more intense reaction. Again, there is a difference in 
the resisting-powers of different types of cells. Thus the motor cells of 
the anterior horn are iDCCuliarly resistant to injury to their axones, as 
are also the spinal ganglion cells to injury to their central processes. 
Again, between cells of the same type there are marked variations in re- 
sisting-powers. Thus the motor cells of the anterior horn are much more 
resistant than the cells of the motor cranial nuclei. ' 

' For review and bibliography of changes in the nerve cell and in the proximal stump 
after section of a peripheral nerve consult Barker, " The Nervous System, " p. 229 et seq. 



the neeyous system. 737 

((1) Changes in the Cell Body Eesultino from Lesions to its 
Dexdeites. — In the study of the effect upon the cell body of a lesion 
depriYiug it of one or all of its dendritic processes, we meet with the 
same experimental obstacles already mentioned in connection with 
changes in the dendrites. It is, again, only in the peripheral arm of the 
spinal ganglion cell that we have a cellulipetal process of any consider- 
j able length. Section of this process resnlts in changes in the spinal gan- 
glion cell cpiite similar in character to the so-called ^^axonal^' degenera- 
tion (Plate XIII., 6). If we consider that a cell's dendrites furnish its 
only or at least its main avenue for the reception of impulses, it follows 
that a neurone is thrown as comx)letely out of circuit, as it were, by in- 
jury to its dendrites as by injury to its axone. The exj)eriments of 
AVarrington ' are interesting in this connection. He attempted to bring 
about the same functional effect as would result from section of a cell's 
I dendrites, by inhibiting afferent impulses. Cutting the posterior roots, 
he noted changes in the cells of the anterior horn. The inference was 
that these changes were induced by an inhibition of the customary nor- 
mal stimulation by means of the afferent impulses reaching the cells 
through their dendritic processes. 

II. Changes in the Neurone from Interference with its Nutrition. — 
Changes apparently of a degenerative character have been described in 
neurones as a result of interference with nutrition. Thus Brieger and 
Ehrlich ^ found that by temporarily 'applying a ligature to the abdominal 
aorta, they induced an acute necrosis of the cells of the lumbar cord. 
Later experiments of a similar nature followed by the Marchi staining 
showed that the degenerative process affected not only the cell bodies, 
but the entire neurone. Similai^ degenerative changes have been induced 
by exi)erimentally produced multiple emboli, cells in the vicinity of the 
occluded vessels being in marked contrast to cells from regions whose 
vessels remained patent. Ewing' describes marked degenerative changes 
in nerve cells as a result of anaemia consecutive to pressure from cere- 
bral hiemorrhage and to thrombosis of the basilar artery. Less marked 
changes have been observed in cases of general malnutrition and in se- 
vere anaemias. 

III. Effects of Toxins upon Neurones. — Changes of a degenerative char- 
acter occur in neurones as a result of the action of toxins. These toxins 
may be introduced into the body from without, for example, such poi- 
sons as alcohol, arsenic, lead, strychnine, etc. ; they may be elaborated 
within the body as the result of faulty metabolism, for example, ursemia, 
eclampsia, etc. ; or as a result of the action of bacteria, as in tetanus, 
rabies (Plate XIIL, 3, 4, and 8), diphtheria, etc., or of the Plasmodium 
malaria. The effects of these poisons upon the neurone vary with dif- 

^ Warrington, W. B., "On the Structural Alterations in Nerve Cells." Jour, of 
Physiol., London, vol. xxiii., 1898. 

"-Brieger unci Ehrlich. "Ueber die Ausschaltung desLendenmarkgrau." Zeitschr. f. 
klin. Med., Berlin. Bd. vii., Suppl., 1883-84. 

'■'Ewing, J., "Studies on Ganglion Cells." Arch, of Neur. and Psychopath., vol. i., 
1898. 

47 



738 THE NERVOUS SYSTEM. 

ferent poisons and in different types of neurones. The effects of the 
same poison upon a given type of neurone also vary according to its 
rai^idity of action, whether rapidly fatal or extending over a considerable 
period of time. Again, given the same poison and the same time of 
action, not all neurones even of the same type show an equal suscepti- 
bility. There seem to be marked individual differences among neurones 
of the same type as regards their resisting powers. 

These changes in the neurone from the action of toxins may affect one 
or all of its structural elements, and vary from the slightest appreciable 
loss of staining qualities of the chromox)hilic bodies to complete destruc- 
tion of the neurone. In the chromophilic bodies the essential change 
seems to be a decrease in the amount of chromatic substance, chromatol- 
ysis. This may be evidenced merely by a decreased staining intensity, 
the chromatic masses appearing abnormally pale ; the bodies may have a 
ragged or frayed -out appearance at their edges ; they may be shrunken, 
or, retaining their normal shape and size, become vacuolated (Plate 
XIII., 3) ; they may completely disintegrate, giving to the cell a diffuse 
granular appearance ; they may disappear, leaving the cell entirely devoid 
of chromatic substance. The chromatic masses in the dendrites seem in 
many cases to be more resistant or less exposed than are those in the body 
of the cell, often remaining unchanged at a time when the latter show an 
advanced degree of chromatolysis. During these changes in the chro- 
matic element the cyto- reticulum may remain apparently normal or it 
may more or less completely disintegrate. This disintegration usually 
marks the more advanced degenerative changes (Plate XIII., 4). 

In the truly achromatic element of the cell or cytoplasm, our present 
methods of staining fail to demonstrate lesions. Diffuse staining of this 
basement substance is a common phenomenon of chromatolysis, but seems 
more properly referable to a diffusion of the fine granules resulting from 
disintegration of the chromatic masses than to any change in the cyto- 
plasm itself. Disappearance of the formed elements of the cell often 
leaves clear holes or vacuoles in the cell body or gives the appearance of 
cracks or fissures. The nucleus may remain normal ; it may swell and 
its contour become abnormally distinct ; it often takes a diffuse stain ; 
later it shrinks, becomes crenated, its reticulum and limiting membrane 
break up and its outline is lost. During these nuclear changes the nu- 
cleolus may also disintegrate. It is often extremely resistant, remaining 
apparently unchanged after most of the other parts of the cell have be- 
come unrecognizable. Concurrent with these changes in internal struc- 
ture are changes in the shape and size of the cell. Its contour becomes 
irregular, and its edges present an eroded appearance; the cell body 
shrinks away from its cell space, breaks up, and ultimately disappears. 
The dendrites undergo alterations similar to those in the body of the cell. 
They shrink, become separated from the cell body, and finally disinte- 
grate. 

To the action of a specific poison certain neurones seem less resistant 
than others. Thus, to the action of lead those neurones governing the 



THE XERYOUS SYSTEM. .739 

extensor muscles of the wrist seem especially susceptible. The cells of 
the motor uucleus of the trigeminus seem to be less resistant than other 
motor cells to the poison of tetanus. Again, the frequency with which 
tabes dorsalis is associated with a syphilitic history seems to indicate a 
special susceptibility to the sj^philitic poison on the iDart of the peripheral 
sensory neurone. 

Comparing the changes in the nerve cell in toxaemias (Plate XIII., 3 and 4) with 
those induced b}^ lesions to its axone — axonal degeneration (Plate XIII. , 6) — we note 
that while in the latter the chromatolysis is central in character, beginning in the region 
of the axone hill and nucleus, in the former the changes begin at the periphery, the 
portion of the cell in most direct relation to the surrounding Ij^mph. In axonal de- 
generation the nucleus is usually eccentric. In toxaemia it usually remains central, at 
least until the process of degeneration is far advanced. 

IV. EiFects of Fatigue upon Neurones. — Studies upon the effect of fa- 
tigue ui)on the neurone haYC been made in animals after prolonged mus- 
cular activity and after electrical stimulation. ^Tiile the results are not 
in complete accord, there seems to be little doubt that definite mori)ho- 
logical changes occur in the neurone as a result of fatigue. These changes 
consist in a decrease in the size of the cell body, a decrease in the size of 
the nucleus, often with distortion, and a marked decrease in the amount 
of chromatic substance with more or less diffuse staining of both cell 
body and nucleus. 

It seems not at all improbable that the clinical pictures presented by certain psy- 
choses and neuroses are the expression of the effects upon the neurones of prolonged 
fatigue. Certain local expressions of neurone exhaustion, as, for example, writer's 
cramp, may possibly also be placed in the same category. 

As to the significance of those changes in the nerve cell, which are marked hy dim- 
inution in the chromatic substance alone, and to which the term " chromatolysis " has 
been given, there is a considerable difference of opinion. Marinesco^ considers them of 
the nature of degeneration. Van G-ehuchten^ is inclined to look upon the phenomenon 
as conservative in character, a means by which the neurone assumes a condition most 
advantageous for self-defence. It has been shown that even an extreme degree of 
chromatolysis is not incompatible with function. Marinesco insists that so long as the 
changes are confined to the chromatic substance recovery is possible, no matter how 
extensive the alterations, while changes in the achromatic elements are always per- 
manent in character. It seems quite probable that a comparatively easy method of 
investigation has led to an overestimation of the significance of changes in the chro- 
matic substance of the neurone, and to a neglect of probably more important but less 
easily studied changes in the achromatic element. 

EegexeeatioNo 

Eegeneration of nerve tissue in the sense of an actual reproduction 
of neurones probably never occurs in the adult human nervous system. ' 
As has been noted, extreme chromatolysis may be succeeded by complete 
recovery. In the case of axonal chromatolysis, the degenerative process 

^ Marinesco, G., See Van Gehuchten's "Anatomic du Svsteme Nerveux," p. 339. 

2 Yaji GehncTiten, loc. cit., p. 339. 

3 For review and literature on "Regeneration," see Barker, "The Nervous System," 
p. 245 et seq. 



740 THE NERVOUS SYSTEM. 

usually reaches its maximum in about three weeks. Reformatiou of 
chromophilic bodies theu begius. This recoustructive process is slow, 
the cells ofteu requiring months to return to a normal condition. At 
some stage of the process there is usually an over-production of chro- 
matic substance, and the cells appear darker than normal. 

Primary union between the ends of divided nerve fibres does not 
occur. Complete degeneration of the distal iDortion always precedes the 
regenerative process. In this reconstruction the nuclei of the neurilemma 
seem to play an important part. They increase in number, and there is 
also an increase in the protoplasm which surrounds them. With union 
of the divided ends the axoues of the central stump may grow out again 
if the ganglion cells be intact, and ultimately resume function. The 
myelin first reappears as droplets which coalesce and finally form a 
complete sheath. This reconstructive process in the nerve fibre is ex- 
tremely slow, often requiring many months for its completion. 

Eeplacement ^Neuroglia Hyperplasia. — Under various condi- 
tions in which there is destruction of the parenchyma, as, e.g., in ascend- 
ing and in descending degeneration in the spinal cord, there occurs a 
compensatory increase in the interstitial elements. This new tissue is at 
first cellular, most of the cells being of the spider variety. Later there 
is an increase in the neuroglia fibres, and the tissue often becomes dense 
and hard. What part the mossy cells or other less common types of 
neuroglia cells take in the proliferative process is as yet unknown. 
With the increase in fibres there are often shrinkage and the formation of 
dense fibrous tissue. This replacement hyperplasia in neuroglia seems 
quite similar in nature to replacement connective-tissue hyperplasia in 
other organs, and is often considered inflammatory. 



Degeneratio?\'s Affecting Systems of Neurones. 

General Considerations Concerning Neurone Systems. 

Before considering the subject of systemic degeneration we may refer briefly to 
the situation in the nervous system of certain of the more important groups of neurones 
and the paths whicli their axones take. 

That the cell bodies of neurones are grouped in the gray matter of the brain, cord 
and ganglia, and in the end organs of certain nerves of special sense, has already been 
mentioned. This grouping of neurones serves definite physiological ends. Their cell 
bodies form centres or nuclei, while their axones are collected into bundles or fibre 
tracts. Thus, in the region of the fissure of Rolando are grouped the centres of those 
neurones which have to do with voluntary motion, and what is known as cerebral local- 
ization means the grouping of cell bodies of neurones for specific function. After the 
known localizations are eliminated, there still remains unaccounted for the greater part 
of the cerebral cortex, and our present belief is that these neurones are neurones of 
association by which the various centres are brought into physiological relationship. 
Some understanding of this neurone grouping, and especially of the arrangement of 
th€'ir neuraxones as fibre tracts of the cord is essential to an appreciation of those 
degenerations which affect definite systems of neurones. 

Peripheral Motor Neurones. — These neurones have their cell bodies in the gray 
matter of the anterior horn and in the motor nuclei of the cranial nerves. Their neur- 



THE NERVOUS SYSTEM. 741 

axones pass out as the motor fibres of the cranial and of the spinal nerves. The entire 
neurone lies upon the same side of the body ; that is, the peripheral motor neurone is 
" direct. " 

The Upper oh Cortico-Spinal Motor Neurones have their cell bodies situated 
mainly in the cerebral cortex near the fissure of Rolando. Their neuraxones converg- 
ing, pass through the internal capsule, pons, and medulla, sending off fibres to the 
motor nuclei of the cranial nerves. In the medulla the tract comes to the surface as the 
anterior jyyramids. At the junction of medulla and cord occurs the pyramidal decussa- 
tion in which most of the fibres of the tract cross to the opposite lateral region of the 
cord, to be known as the crossed jyyramidcd tract, while a minority remain on the same 
side, to pass down the cord as the direct pyramidal tract. As the tracts descend, fibres 
continuously leave them to terminate, those of the crossed tract in the gray matter of 
the same side, those of the direct tract, after jDassing through the anterior commissure, 
in the gray matter of the opposite side. The cortico-spinal motor tract is a crossed 
tract. 1 These tracts present variations in size and length. They are often asymmetrical. 
The crossed tract extends to the lower sacral cord. The direct tract usually ends about 
the mid-dorsal region, though it has been followed as low as the second lumbar segment. 

The Sensory Afferent Tract, like the motor, consists of two segments, an 
upper and a lower. 

The loicer or periiiilieral sensory neurone tract has its cell bodies in the ganglia of the 
spinal and of the cranial nerves. Their peripheral arms, which Van Gehuchten con- 
siders protoplasmic processes, are axis cylinders of cranial or of spinal nerves. Their 
central processes or axones pass into the cord as the fibres of the posterior roots and 
enter the posterior columns. Here they divide into ascending and descending arms. 
The descending arm is short, and with its collateral branches soon terminates in the 
gray jnatter of the same side of the cord. The ascending arm may also be short, and 
with its collaterals terminates as does the descending. It may pass a considerable dis- 
tance up the cord and then end in the gray matter. It may, as one of the long fibres 
of the posterior columns, continue upward to the medulla, where it terminates in one of 
che posterior column nuclei. These long fibres pass inward as they pass uj^ward, so 
that the lower the origin of the fibre the more mesial is its position in the upper part of 
the cord. The entire neurone lies upon the same side of the cord. The lower sensory, 
like the lower motor neurone, is direct. 

Upper Sensory Neurones. — The arrangement of these neurones is extremel}^ complex, 
and only those whose axones enter into the formation of distinct tracts of the cord will 
be here mentioned. Of the above-described central arms of the peripheral sensory neu- 
rones, some of the shorter enter the gray matter of the cord and with their collaterals 
terminate around motor cells (reflexes). Others terminate around cells whose axones 
cross to the opposite side of the cord and pass upM^ard as the antero-lateral ascending 
tract, or tract of Gowers. Other fibres terminate around cells of the column of Clarke, 
the axones of which pass upward as the direct cerebellar tract. 

In addition to these main fibre tracts, there are in all regions of the cord fibres 
which are commissural in character. These fibres are the axones of cells situated in the 
gray matter of the cord, and after passing a short distance up or down and sending col- 
laterals into the gray matter, themselves re-enter the gray matter and terminate there. 
These short fibres make up the so-called ground bundles or fundamental columns of the 
cord. They attain their greatest development in those regions of the cord where the 
reflex centres are most extensive, i.e., in the lumbar and cervical enlargements. 

Secondary Degenerations. 

Secondary degenerations are dei)endent upon the fact already noted 

that the cell body being the troi)hic centre of the nenrone, the axone 

when separated from its cell body dies. 

^ Certain recent observations tend to show that there may be a small number of 
" direct " fibres in the so-called crossed pj^ramidal tract. 



742 THE NEEYOUS SYSTEM. 

Descexdixg DeGtENEEAtion. — Any cortical lesiou, such as embolic 
softening and apoplectic clots, which destroys the uerYe cells, or any 
lesion of the brain or cord which interrnpts the axone tracts of the 
cortico- spinal system of neurones, determines a complete degeneration of 
the affected axones (Fig. 437). The course of these axones has been 
described. Thus a lesion of the brain affecting motor neurones is fol- 






-tJ 






riG. 437.— Secondary Descending Degeneration. 

From hiemorrharre into the internal capsule, almost complete degeneration of the direct pyramidal tract 
on the same side as the lesion and of the crossed pyramidal tract on the opposite side. There were a few 
degenerated fibres iu the crossed tract on the same side as the lesion. 

lowed by a degeneration in the motor tract of the same side down to the 
pyramidal decussation, and below that point, in the direct motor tract 
on the same side and in the crossed tract on the opposite side, the num- 
ber of degenerated fibres being proportionate to the number of cells de- 
stroyed or axones interrupted. In a number of cases of descending de- 
generation due to cerebral lesions, degenerated fibres were found in the 
crossed pyramidal tract on the same side as the lesion. This degenera- 
tion was not present in all cases, and in no case was it as marked as the 
degeneration in the opposite lateral tract. The most probable explana- 
tion is that a small number of fibres instead of decussating pass down 
into the cord in the lateral tract of the same side. 

In descending degeneration due to a lesion below the pyramidal de- 
cussation a somewhat different picture is presented. In a complete trans- 
Yerse lesion there is degeneration of both crossed and of both direct pyr- 
amidal tracts. If the lesion is unilateral the degenerations are upon the 
same side as the lesion. The areas of degeneration are also larger and 
less sharply defined than in cerebral lesions. Then in addition to the 
degeneration of the pyramidal tracts there is a degeneration of a con- 
siderable number of fibres in a crescent -shaped area lying near the periph- 
ery of the antero -lateral region and extending from the crossed to the 



THE XERYOUS SYSTEM. 743 

direct tract. Degeneration of these fibres has been described by Marchi ' 
after remoYal of the cerebellum. He considers them descending cere- 
bellar fibres. The so-called comma-shaped degeneration in the posterior 
columns is sometimes present. Schultze^ regards these fibres which 
are situated about the middle of the posterior columns, as descending 
axones of spinal ganglion cells. Tooth ' thinks that they are more prob- 
ably descending branches of commissural neurones. In the fundamental 
columns the degeneration extends but a short distance below the seat of 
injury, and of course affects only those axones which descend. 

AscEis'DiXGr Degexeeatiox. — Any lesion which destroys the spinal 
ganglion cells or which interrupts their axones determines a secondary 
ascending degeneration in the posterior columns (Fig. 4.38 j. Any lesion 
of the cord which interrupts the tract of Gowers or the direct cerebellar 
tract is followed by degeneration of the fibres of these tracts aboYC the 
lesion (Fig. 438). Immediately above the lesion there is complete de- 
generation of the tracts. As we pass upward new undegenerated fibres 
from the spinal ganglia above the lesion enter the column of Burdach, 




X 



# 



'^S: 



// 



FIG. 438,- Secoxdart ascending Degeneration. 

Following complete crushlBg of tbe cord about two segments below the level at which the section was 
taken. Degeneration is almost complete in the columns of GoU, of Gowers, and in the direct cerebellar 
tracts. A few normal fibres are seen in the columns of Burdach, These are the ascending axones of spinal 
ganglion cells bet^'een the point of injury and the level of the section, and are seen to occupy that part of 
the posterior columns adjacent to the posterior horns. 

so that there appears in the iDOSterior columns a constantly increasing 
number of normal fibres. Also in the column of Gowers undegenerated 
fibres appear as one passes upward from the lesion. Some of these fibres 

^JlarcJd, "Origine e decoroso dei peduncoli cerebellari." Rev. Sper. de Fren. e 
Med. e leg., Bd. xvii.. p. 367. 

"- Schultze, "On Comma-sliaped Degeneration of the Posterior Columns. " Arch. f. . 
Psych., 1883. 

^^ Tooth, " Goulstonian Lectures on Secondary Desreneration of the Spinal Cord. " Lon- 
don, 1889. 



744 THE NEEYOUS SYSTEM. 

probably liaYe their origin in the gray matter of the cord, and the num- 
ber of normal fibres is in proportion to the number of these cells be- 
tween the lesion and the i)oint at which the section is taken. Descending 
fibres in these columns have already been mentioned. They, of course, 
do not degenerate. If the lesion be above Clarke's columns the degen- 
eration in the cerebellar tracts remains complete ; if not, the number of 
normal fibres is in proportion to the number of Clarke's column cells 
between the lesion and the point of section. The ascending fibres of the 
fundamental columns also degenerate, but are so short that tliey cannot 
usually be traced beyond the area of direct action of the traumatism. 



Primary Degenerations. 
Degeneration of the Peripheral Motor ^N'eurones. 

Progressive spinal muscular atrophy is the clinical designation of 
a disease, the underlying lesion of which is a progressive atrophy or 
degeneration of the lower motor neurones. There is a degeneration of 
the large motor cells of the anterior horns and of their processes. This 
degeneration goes on to complete destruction of some neurones. With 
the loss of nerve tissue proper there is a compensatory growth of neu- 
roglia. In a well-advanced case section of the cord shows a marked 
diminution in the number of anterior horn cells and an atrophic condition 
of the horn itself and of the anterior roots. The lesion usually begins in 
the cervical region. More rarely it starts in the lumbar cord. The de- 
generation may extend to the motor cranial nerve nuclei, giving the 
picture of a progressive bulbar paralysis. The medullary nuclei most 
commonly involved are the hypoglossal and the spinal accessory. Less 
often the degeneration affects the cells of origin of the fifth and seventh. 
Degeneration of the peripheral nerves has been described. The muscu- 
lar lesions correspond to the lesions in the cord, the muscles of the hand 
and arm being usually first affected. For the degenerative changes in 
the muscles see page 687. This lesion is sometimes described as a 
chronic antero-poliomyelitis. Both its clinical history and its pathology, 
however, indicate the degeneration as the initial lesion and the neuroglia 
increase as secondary — a replacement hyperplasia. 

Degeneration of the Cortico-Spinal Motor IS'eurones. 

Spastic Paraplegia — Spastic Spinal Paralysis. — This may be described as 
a primary lesion of the upper or corticospinal motor neurones. It is 
probable that the lesion affects the entire neurone. As a distinct patho- 
logical entity the condition is extremely rare. Whether it originates in 
a degeneration of the cell bodies of these neurones in the cortex is not 
known. The clinical picture of spastic paraplegia, due to compression, 
to a transverse myelitis, or to a multiple sclerosis, is not uncommouo 



THE NEEYOUS SYSTEM. 745 

Marie' considers spastic paraplegia as a disease appearing in childhood, 
and due to a faulty dcYelopment of the cortico- spinal motor neurones, 
rather than to their degeneration. 

Degeneeation^ of Both Peripheral and Cortico -Spinal Motor 

^NTeurones. 

AmyotrojMc Lateral Sclerosis. — This is a primary progressiYe degener- 
ation inYolving both cortico -spinal and spino -peripheral motor neurones. 
The appearance of the transYcrse section of the cord is a combination of 
that in spastic paraplegia and in progressiYe muscular atrophy. There 




Fig. 439.— Amyotrophic Lateral Sclerosis. 

Degeneration of the crossed pyramidal and of the direct pyramidal tracts. In this case there was but 
little atrophy of the anterior horns. Very few cells, however, were present in the anterior horns and there 
was an increase in the connective tissue of the horns. 

is a degeneration of the cells of the anterior horn with atrophy of the 
horn itself, and a degeneration of the fibres of the direct and of the 
crossed pyramidal tracts (Fig. 439). The lesion in the horns is usually 
pronounced. The extent of iuYolYement of the motor tracts of the cord 
is extremely Yariable. The degeneration in these tracts has been traced 
through the medulla, pons, and cms to the cortex, where changes haYC 
been observed in the large pyramidal cells. In the gray matter of the 
medulla are also found changes analogous to those in the anterior horns, 
consisting in degeneration of the cells of the motor cranial -nerve nuclei. 
The muscle changes are those of a progressive muscular atrophy. 



Degeneration of the Peripheral Sensory ^N^eurones — (Tabes 
DoRSALis— Posterior Spinal Sclerosis — Locomotor Ataxia). 

It seems probable that the essential lesion of tabes is a primary pro- 
gressive degeneration of the peripheral sensory neurones. As its older 

^ Marie, "Lectures on Diseases of the Spinal Cord," London, N. S. Soc, 1895. 



746 THE N^ERVOUS SYSTEM. 

title indicates, the clinical picture of locomotor ataxia had been attrib- 
uted to a primary sclerosis of the posterior columns. This was not be- 
cause in these columns were the only lesions, but because, owing to the 
close packing together here of the sensory axones, this lesion was the 
most conspicuous. 

On removing the cord in a case of advanced tabes, certain changes are 
usually apparent to the naked eye. The pia mater between the two pos- 



Y^ 



FIG. 440.— Tabes Dorsalis. 
Cervical region, showing an early stage of the lesion. 

terior horns is apt to be thickened, of a dull appearance, and adherent 
to the cord. This, in contrast to the normal condition of the rest of the 
pia, gives the effect of a narrow band extending the length of the cord. 
The posterior columns may be depressed, of a grayish color, and firmer 
than the rest of the cord. On section the contrast between the posterior 
columns and the rest of the white matter of the cord is often very dis- 
tinct. In cords removed from cases dying during the earlier stages of 
the disease there are often no macroscopic lesions. 

The microscopic appearances vary, depending on the stage, extent, 
and location of the lesion (Fig. 440). 

In a case which comes to autopsy early in the disease the appearance 
of the lesion differs from that in a case of advanced tabes. As already 
noted, the most marked changes are in the posterior columns. In the 
more common tyiDe of the disease in which the degeneration begins in 
the lumbar region, sections of the cord in this region show certain quite 
well-defined areas of degeneration. The zone of Lissauer early shows 
marked degenerative changes. This zone extends across the entering 
fibres of the posterior root which divide the zone into two parts. The de- 
generation of the outer part has been wrongly described by some writers 
as a lateral -column degeneration. It will be remembered that these 
fibres are short fibres which have entered the cord in the nearest posterior 
root. Degeneration usually appears early in that part of the column of 
Burdach which borders the posterior horn. The column of Goll varies 



THE NERVOUS SYSTEM. 747 

as to the extent of involvement. In many cases it is only slightly af- 
fected, in others the degeneration is marked. As the fibres of this col- 
umn come mainly from the last lumbar and first two sacral segments, it 
is seen that its condition depends entirely upon the integrity of these 
roots. The fibres of the posterior columns have two sources: (1) enter- 
ing fibres of the posterior roots; (2) fibres from cells in the gray matter 
of the cord. The latter are situated mainly in a narrow strip behind the 
posterior commissure and in the median oval area of Flechsig. These 
fibres are unaffected in tabes. 

The appearances of cross sections in the dorsal and cervical regions 
in lumbar tabes are dependent upon an ascending degeneration of the 
fibres affected below. The columns of Goll are thus usually affected, 
while the columns of Burdach are often only slightly involved. If at 
any level of the cord degenerated root fibres enter the cord, there results 
a degeneration in the zone of Lissauer and in the band of fibres lying 
along the posterior horn at that level. 

Earely the tabetic process begins in the cervical region. In these 
cases section of the cervical cord shows not only normal endogenous 
fibres, but a normal condition of the column of Goll and of such part of 
the column of Burdach as originated below the level of the lesion. Some- 
times the dorsal roots are affected with the cervical. The lesion may in 
any case be asymmetrical, one root of a segment being affected while the 



A 



1 



Fig. 441.— Tabes Dorsalis. 
Cervical region, showing an advanced stage of the lesion. 

other remains normal. Marie describes a variety of tabes in which the 
lesions begin in the cranial nerves. 

In cases of advanced tabes (Fig. 441) there are often almost no nor- 
mal nerve fibres in the posterior columns, the columns of Goll, of Burdach, 
and of Lissauer presenting little but dense fibrous tissue. The posterior 
fissure may be completely obliterated. There usually remain, however, 
even in advanced tabes, undegenerated fibres bordering the posterior com- 



748 



THE NEEYOUS SYSTEM. 



missure aud the adjacent parts of the posterior horns. In the lumbar 
regions the median area of Flechsig also remains intact. As already 
noted these fibres are endogenous. 

The microscopical appearance of the degenerated areas Yaries with the 
stage of the process (Fig. 442). The new connectiYe tissue may be at 
first quite cellular; later the fibrillar elements predominate and the 
tissue becomes dense and firm. Of the nerYe fibres some haYC disap- 
peared, others show degeneration of their medullary sheaths and axis 
cylinders. Some few normal fibres are usually present even in advanced 
sclerosis. The blood-Yessels often have thickened walls. There may be 














Fig. 442.— posterior Spinal Sclerosis. (Tabes dorsalis.) 

A portion of sclerosed area in the posterior columns of the spinal cord, a, New-formed connective tissue; 
b, blood-vessels ; c, nerve fibres ; d, atrophied nerve fibres. 



corpora amylacea and fat globules, the latter either free or collected in 
cells. 

The lesion of tabes is not, however, confined to the posterior columns. 
The posterior horns are usually smaller than normal, with a marked re- 
duction in the number of fibres entering them from the posterior col- 
umns. According to the researches of Lissauer, ^ the columns of Clarice in 
the dorso-lumbar region show a diminution in the number of delicate 
fibrils which under normal conditions surround the ganglion cells. Atro- 
phy of the posterior roots almost always occurs. Under the microscope 
there is seen a great reduction in the number of entering fibres. Similar 
atrophy may affect the sensory roots of the cranial nerves. Degenerative 
changes in the cells of the posterior root ganglia have been described in a 
number of cases. In Plate XIII., 7, is seen a portion of a spinal 
ganglion from a case of advanced tabes. In addition to the degenera- 
tion in the cells present there was a marked reduction in the number of 
cells in the ganglion. 

^ Lissauer, Fortschritte der Medicin, Bd. ii., No. 4, 1884. 



THE XEEVOUS SYSTE3I. 749 

Degeneration of the peripheral nerves is of frequent occurrence in tabes 
and, like similar conditions due to toxic agents, is usuallj^ referred to 
as a neuritis. The changes are usually most pronounced in the smaller 
peripheral branches. Degeneration of the 0]3tic nerve — optic neuritis, 
so called — occurs in from ten to twenty per cent of cases. There may 
be changes in the nerve cells of the retina. The same condition in the 
auditory nerve is less frequent. Changes have been described in the spi- 
nal root of the fifth cranial and in the fasciculus solitarius which consists 
of afferent fibres of the vagus and glossopharyngeal nerves. Changes 
have been observed in the peripheral sensory end organs. Degeneration of 
the eeJls of the anterior horns has been noted by Condoleon.' This has 
been accepted by some investigators as explanatory of the various trophic 
disturbances which so frequently occur during the course of tabes. Sim- 
ilar changes have been found in the nuclei of two of the motor cranial 
nerves, the oculomotor and the hy]3ogiossaL Others ascribe the trophic 
disturbances to a peripheral neuritis. Marie^ describes a case interest- 
ing in this connection, in which there was marked hemiatrophy of the 
tongue with distinct changes in both main and accessory nuclei of the 
hypoglossal ner^ e on the same side, the opx)Osite nuclei being normal. 
Oppenheimer describes a similar case of tabes with laryngeal crises in 
which there wfere pronounced degenerative changes in the pneumogastric 
nucleus and in the ascending root of the glossopharyngeal. Changes 
have been described in the cells of the cerebral cortex. They are similar 
to those found in dementia paralytica, but less marked. 

Althoiigli Tarious hypotheses have been advanced in explanation of the tabetic 
lesion, and especially in reference to the fairly constant selection of certain groups of 
neurones, doubt still exists as to the origin and essential nature of the process. Earlier 
writers looked upon the lesion as a primary sclerosis of the posterior columns, probably 
of vascular origin. Flechsig^ and Trepinski '^ describe the posterior columns as made up 
of several distinct sj^stems of fibres, each system distinguishable from the others by its 
period of ripening or myelinization. They assert that the tabetic process affects these 
different systems successively. As the systems overlap one another, this would explain 
the admixture at certain stages of tabes of normal and abnormal fibres. Present 
knowledge favors the view that tabes is a primary degeneration of the peripheral sen- 
sory system of neurones, the degeneration affecting the entire neurone, and that the 
picture presented by the tabes cord varies with the particular neurones affected. The 
cell bodies of these neurones are in the spinal ganglia and theii' cranial analogues. 
Thorough examinations of spinal ganglion cells have as yet been made in too few cases 
to warrant any general conclusions. Degeneration of spinal ganglion cells in tabes has 
been reported even in cases dying early in the disease. Such degenerations are best 
shown by the method of Nissl, the general application of which is comparativeb'' 
recent. Certain it is that a' degeneration which affects both peripheral and central proc- 
esses of the neurone, and yet is most pronounced in those parts of the neurone farthest 
removed from its nutritive centre, is most easily explained on the basis of some agent 

^ Comloleoii, "Contribution it I'etude pathogenique de I'amyotrophie tabetique." 
These de Paris. 1887. 

'^ Marie, loc. cit., p. 258. 

^ Flechsig. ''Die Leitungsbahnen im Gehirn und Ruckenmark," Leipsic, 1878. "1st 
die Tabes Dorsalis eine System Erkrankung? " Neur. Cent., Bd. ix. 

^ TrepinsJd, " Die embryonalen Fasersysteme in den Hinterstrangen und ihre 
Degeneration bei der Tabes Dorsalis." Arch. f. Psych, und Xerv., Bd. xxx., 1897. 



750 THE K-EEYOUS SYSTEM. 

affecting the general metabolism of tlie neurone. A majorit}" of the cases of tabes give 
a syphilitic history. Our knowledge of the effects of toxins upon neurones is certainly 
not opposed to the consideration of such a toxin as the etiological factor in tabes. 

Combined Sy^stem Degeneration — Ataxic Paraplegia. — This is 
a disease of uncertain etiology, in which there are degeneratiYe changes 
in both motor and sensory neurone systems (Fig. 443). The tracts usu- 
ally iuYolYed are those of Burdach and of Goll, the direct cerebellar 
tracts, and the crossed pyramidal tracts. Less commonly the degenera- 
tion extends to the tracts of Gowers and to the direct pyramidal tracts. 
It seems probable that the lesion in the cord is not always the expression 




Fig. 443.— Combined System Disease. 

Showing: degeneration and sclerosis in the columns of Goll, the direct and the crossed pyramidal tracts, 

the direct cerebellar tract. 



of the same pathological process, and that in many cases it is not the 
result of a true systemic degeneration. In perhaps the minority of cases 
the lesion corresponds to the tract systems of the cord and probably 
represents a combined sensory-motor degeneration. Such are those rare 
cases in which the degeneration affects all of the above-mentioned tracts. 

According to Dejerine, the appearance of a combined system disease may be 
induced by the chronic meningitis, which exists over the posterior columns in tabes, 
extending forward over the direct cerebellar tract, the productive inflammation finally 
spreading to this tract and to the crossed pyramidal. In these cases that part of the 
latter tract which lies deepest, i.e., close to the gray matter, usually remains unin- 
volved. Marie lays particular stress upon the arterial systems of the cord as the prime 
factor in many cases, calling attention to the fact that the lesion, as it is most commonly 
found, coincides almost exactly with the distribution of the posterior spinal arteries. 
By others the lesion is ascribed to a multiple sclerosis, the restriction of the degeneration 
to definite tracts being only apparent. It is possible that in some cases the patho- 
logical picture of a combined sclerosis may be due to secondary degeneration following 
myelitis. 

A subacute type of combined system degeneration has been described by Russell.^ 
The degeneration involved the same tracts affected in the more chronic type, and was 

1 Brain, Spring, 1900, vol. xxiii.. No. 89. 



THE XERYOUS SYSTEM. 751 

often very extensive at some levels of the cords studied, tliere being only a thin layer 
of normal fibres covering the gray matter. 

Under the name of diffuse degeneration of the spinal cord, Putnam and Taylor' 
describe a somewhat similar condition, leaving open the question as to the systemic 
nature of the process. 



Friedreich's Ataxia. (Hereditary Ataxia. ) 

This disease while often referred to as hereditary ataxia, has more of 
a family than of a distinctly hereditary character. Its pathology is 
marked by a decrease in the size of the spinal cord, the diameter of which 
is often not more than three -quarters that of the normal cord. Degen 
eration of the columns of Goll is usually quite complete. Less marked 
degeneration is found in the columns of Burdach, in the direct cerebellar 
and in the crossed pyramidal tracts. The marginal tract of Lissauer may 
or may not be affected. In the posterior horns and in the columns of 
Clarke the condition resembles that in tabes. There may be atrophy of 
the cerebellum. 

Marie notes in addition, atrophy and disappearance of the cells of Clarke's column. 
Blocq and Marinesco- describe degeneration of the posterior root fibres similar to that 
found in tabes. Friedreich ^ and Riitimeyer'* find atrophy of the anterior horn cells. 
The determining cause of the disease and the nature of the morbid process are as yet 
undetermined. It seems probable that the condition of the cord jnaj be more properly 
considered an abnormality of development rather than a degeneration. 



Cerebellar Ataxia. 

Atrophy of the cerebellum was noted as sometimes occurring in Fried- 
reich's ataxia. In that disease, howcYcr, the cord lesion was most 
marked. In cerebellar ataxia the lesion of the cord is slight or absent, 
the chief lesion being an atroj)hy of the cerebellum. This atrophy is 
accompanied by little or no sclerosis, the organ being simply smaller 
than normal. 

INFLAMMATION. 

Inflammation of the Brain. {Encephalitis.) 

Acute Encephalitis, — Inflammatory processes in the nerYOus system, 
whether of an exudatiYC or of a productiYC type, are frequently consecu- 
tive to or coincident with the more scYcre forms of degeneration or other 
lesions, thus making differentiation of the processes often extremely dif - 

^ Journal of Kerv. and Ment. Disease, Januar}^ and Februarj^ 1901. 
2 Blocq, P. and Marinesco, G., " Sur I'Anatomie Pathologique de la Maladie de Fried- 
reich." Compte rend. Soc. de Biol., 1890. 

^ Frieclreicli, N., Virchow's Archiv, Bd. 86, 1881. 
^Eutimeyer, L., Virchow's Archiv, Bd. 110, 1887. 



752 THE N^EEVOUS SYSTEM. 

ficiilt. It has been already mentioned that the brain tissue about haemor- 
rhages and areas of embolic and thrombotic softening may nndergo in- 
flammatory changes leading to the formation of new connective tissue. 
There is a class of cases in which localized areas of the brain undergo 
softening, Avith more or less extravasation of red and white blood cells 
and hypersemia, so that the softened material consists, as seen under the 
microscoj)e, of detritus of brain tissue in a condition of fatty degenera- 
tion, often with more or less pus cells and j)igment. When such areas are 
red in color from intermingled blood cells or pigment, the condition is 
called red inflammatory softening. When fatty degeneration prevails, and 
the red blood cells or their derivatives are not abundant, the softened 
area looks yellow or yellowish-white, and this is often called yellow in- 
flammatory softening. The origin of these processes is very obscure and 
their inflammatory nature not well defined. 

Abscess of the Brain. — Small multiple abscesses of the brain may 
occur in pyaemia. Large abscesses of the brain are usually single ; they 
may attain a large size. They are most frequent in the cerebral and 
cerebellar hemispheres, rare in the basal ganglia, the pons, and the 
medulla oblongata. 

There may be an irregular cavity containing thin jjus and softened 
brain tissue. The walls of the cavity are ragged and infiltrated with 
pus, and outside of the walls is a zone of oedematous and softened brain 
tissue. If the abscess be near the pia mater, meningitis may follow ; if 
it be near the lateral ventricles, it may rupture into them ; if it be near 
the sinuses of the dura mater, it may induce thrombosis. An abscess 
may in time become enclosed in a capsule of connective tissue. 

Abscess of the brain is most frequently secondary to chronic supi)u- 
rative otitis (42.5 per cent, Gowers), much less frequently to acute otitis. 
With the otitis there may also be caries of the temporal bone, suppura- 
tion of the mastoid cells, and inflammation of the dura mater. The 
abscess is usually situated deep in the brain, commonly in the temporo- 
sphenoidal, the frontal, the occipital or the parietal lobes, or in the 
cerebellum; rarely it is continuous with the inflamed dura mater and 
bone. Abscess may follow chronic lesions in the orbit or caries of vari- 
ous parts of the cranial bones. 

Abscess of the brain frequently follows traumatism, blows, or falls 
on the head. Such injuries may not damage the skull, or may produce 
fractures or necrosis. There is often a considerable interval betweeir 
the time when the injury is inflicted and the development of the symp- 
toms. 

AYhen the cranial bones are uninjured the abscess is usually deep in 
the brain ; when there is necrosis of the bones the abscess may be super- 
ficial ; when the bones are fractured the abscess may be either superficial 
or deep. The abscess develops rarely in the opposite side of the brain. 

In acute exudative meningitis from various excitants there may be an 
infiltration of the brain with leucocytes ; this may be especially marked 
in the perivascular tissue and around the ganglion cells. 



THE XEEYOUS SYSTEM. 753 

An Acute Disseminated Encephalitis, ' h hematogenous iu character, may 
develop during the progress of an infectious disease. It is most com- 
mon in infective endocarditis, in pjEemia, and in epidemic cerebrospinal 
meningitis. It may be associated with acute anteropoliomyelitis, ap- 
parently due to the same obscure etiological factor. The lesion consists 
in disseminated foci of inflammation, or minute multix^le abscesses. 
Some of these are microscoi^ic in size, others may be seen vrith the naked 
eye. The smallest show simx)ly small-round-cell infiltration of the walls 
of one or more small vessels and of the surrounding tissue. The larger 
spots, which undoubtedly take origin in the same way, are seen to be 
softer than the rest of the tissue, and resemble red or yellow softening, 
according to the amount of red blood cell extravasation. Congestion is 
usually marked. There may be distinct haemorrhages. Degenerative 
changes with disintegration of the exudate usually set in and determine 
destructive changes in the neighboring neurone and neuroglia elements. 
At the periphery of one of these abscesses the neuroglia, instead of being 
in a degenerating condition, usually shows i)roliferation. In the case of 
one of the more minute inflammatory foci complete resolution may 
occur with absor]3tion of the exudate. In the larger abscesses there may 
be absorption of the exudate and of the products of degeneration, and 
a replacement neuroglia hyiDerplasia, ultimately resulting in a sclerotic 
patch. 

Suj)purative encephalitis may occur as a result of traumatism or from 
extension of suppurative meningitis. 

A form of encephalitis which has been designated acute non-suppu- 
rative hsemorrhagic encephalitis, has been described by StriimiDell, Leich- 
tenstein, Oppenheim, Putnam,^ and others. The lesion consists in the 
occurrence of multixDle hsemorrhagic, inflammatory foci, which are non- 
suppurative, and which are accompanied by leucocj tic infiltration. These 
foci may occur in any i)art of the brain, but are most numerous in the 
white matter of the brain and basal ganglia. Some of these haemorrhages 
may be quite large. 



Acute IxFLA:\mATiox of the Spinal Coed. (Acute Myelitis.) 

Inflammation in the spinal cord is quite analogous to inflammation 
in the brain. 

Acute Disseminated Myelitis' runs a rapid course and proves fatal in a 
short time. The inflammation may involve nearly the whole length of 

* Under the bead of "Acute Parenchymatous Encephalitis " has been described a 
lesion of the ganglion cells without vascular or interstitial changes. These lesions are 
the result of toxaemias of either endogenous or exogenous nature. They are more prop- 
erly classed as parenchymatous degeneration. 

-Putnam, Jour, of Xery. and Ment. Dis., yol. xxiy., 1897, bibliography. 

2 Acute parenchymatous myelitis, like its analogue in the brain, is a lesion of the 
ganglion cells, and is more properly classed as a degeneration. Embolic and throm- 
botic softening are more rare in the cord than in the brain, and are necessarily much 
more restricted in extent. AVhen of an inflammatory character they resemble the simi- 
lar brain lesion and are red or yellow according to the amount of extravasation. 
48 



754 



THE NERVOUS SYSTEM. 



the cord, but is usually more iuteuse in some places thau in others. The 
cord is swolleu aud congested, it is infiltrated with pus cells, the connec- 
tive tissue is swollen, and there is degeneration of the nerve elements 
proper. 

More frequently an acute myelitis is more localized. It involves but 
a small portion of the length of the cord, while laterally it may com- 
pletely cross it, and is hence spoken of as a transverse myelitis. When 
the cord is removed and laid upon the table, if the lesion is marked, a 
flattening of the cord at its seat may be observed ; or on passing the 
finger gently along the organ, the affected segment will be found softer 
than the rest of the cord, sometimes almost diffluent. On making a sec- 
tion through the affected portion the 
nerve tissue may appear white or red 
or yellowish or grayish. ' 

Microscopical examination shows 
different ai)pearances, depending 
upon the stage of the degenerative or 
inflammatory process. There may be 
much blood, or, if the lesion has 
existed for some time, blood pig- 
ments ; also fragments of more or less 




Fig. 444.— Degenerated Tissue from Acute 
Myelitis. 



desfenerated nerve fibres and 



gan- 



glion cells (Fig. 444), myelin drop- 
lets, free fat granules, and larger and 
smaller cells filled with fat granules (Gluge's corpuscles), pus cells, gran- 
ular matter, neuroglia cells, and sometimes corpora amylacea. The vari- 
ous combinations of these elements give rise to the different gross ap- 
pearances which the diseased part presents. In earlier stages of the 
lesion the blood-vessels may be dilated, the nerve fibres and cells swollen ; 
or the walls of the blood-vessels may be thickened or fatty, or surrounded 
by a sheath of leucocytes and cells derived from the connective-tissue 
cells of the adventitia. 

The lesion is apt to commence in the gray matter or at its edge, and 
then extend first laterally and afterward upward and downward. 

In a certain number of cases the degenerated material may be absorbed 
and a cicatrix or cyst formed. After the least extensive forms of the 
lesion there may be a restoration of the functions of the cord. 

Secondary degeneration, both ascending and descending, may occur 
in this form of myelitis, varying in extent according to the size of the 
primary lesion. The terms central myelitis, peripheral myelitis, and U7ii- 
lateral myelitis, are sometimes used to designate localizations of the lesion. 

Poliomyelitis Anterior — Myelitis of the Anterior Horn. — This name is 
applied to a group of cases which are characterized by clinical symptoms 



^ It should be remembered that a mechanical injury to the cord in removal, such as 
crushing or bruising, may reduce the injured portion to a pulpy consistence and thus 
produce appearances somewhat similar to those of some forms of inflammatory soften- 
ing. See reference to Yan Gieson, on Artefacts of the Nervous System, p. 717. 



THE XERYOUS SYSTEM. 



755 



indicating changes in the anterior horns. The disease is most common 
in children, nnder the name of infantile sjnnal paralysis, bnt occurs also 
in adults. It usually begins with symptoms of an acute infectious dis- 
ease, the paralysis su]3erYening after a few days. It Yaries in acuteness, 
scYcritj', and duration. In many cases there is complete recoYcry, and 
then we must suppose that the changes in the nerYOus tissue were not 
destructiYC in character. In other cases the symptoms are more perma- 
nent, indicating a destructiYC lesion. 

At first a considerable grouj) of muscles, usually of the arms or legs, 
is affected. Eesolution taking place, there may be complete disappear- 
ance of the paralysis. More commonly there is return of function in 
most of the muscles, while some few remain permanently paralyzed and 
become atrophied. The lesion is most frequent in the lumbar and cer- 







Fig. 445.— Poliomyelitis Anterior. 

A, Normal ganglion cells surrounded by nerve fibres: B, degenerated ganglion cells; C, granular masses 
at place of ganglion cells ; D, small cavity containing fluid. 



Yical enlargements, but may occur anywhere, and is often found in scat- 
tered x>atches. Earlier autopsies were in cases of long standing, and 
the changes found consisted in degeneration (Fig. 445), shrinkage, pig- 
mentation, and atrophy of the ganglion cells of the anterior horns, an 
increase in the connectiYC tissue of the cornua and of the adjacent white 
matter, often with destruction of considerable portions of the horns, 
atrophy of the anterior roots, and distortion of the cord. 

Instead of this shrinkage and atrophy of the horns there is sometimes 
found, especiall}^ if the case come to autopsy not too long after the onset, 
a gelatinous condition of the horns, the X)lace of the horns being occupied 
by young neuroglia tissue Y'ith many branching cells and fine delicate 
fibrils resembling glioma (Fig. 446). This gliomatous tissue may break 
down, forming a caYity surrounded by young neuroglia tissue. More re- 
cently autopsies made early in the course of the disease show that the 
changes described aboYe represent only later stages of what originated 



756 



THE NEEYOUS SYSTEM. 



as an acute inflammatory process. Examiuation of the cords from such 
early cases shows congestion, exudation of leucocytes into the iDeriYas- 




FIG. 446.— ACUTE ANTERIOR POLIOMYELITIS. 

Death seven weeks after onset. Showing gliomatous tissue in both horns, with cavity formation in one of 

them. 



.^^ 



^4la^ 



cular and nerYC-cell spaces, and proliferation of the neuroglia. Degen- 
eration of the nerYC cells occurs, probably secondary to the inflammatory 
lesion. The inflammation is similar to that of an ordinary acute mye- 
litis, but seems to be confined 
mainly to the area of distribu- 
tion of the anterior spinal artery. 

In about one-third of the 
cases which are clinically in- 
cluded under acute anterior po- 
liomyelitis, the onset is without 
fever, and there is at no time 
any CYidence of the existence of 
an inflammatory process. While 
thrombosis of a branch of the 
anterior spinal artery or haemor- 
rhages into the anterior horns 
have been suggested in explana- 
tion of these cases, their i)atholo- 
gy remains as yet undetermined. 

Acute Ascending" Paralysis — 
Landry's Paralysis. — This is a 
rare disease characterized clini- 
cally by a rapidly ascending 
paralysis, beginning in the lower 
extremities and progressing up- 
ward to involve the body, arms, 
and head. Until recently no 
pathological changes were 



\t 




ml^l 



1/ 4'\ 



ZI3 



'4k^aK 



Fig. 447.— Landry's Paralysis. 

Section of spinal cord showing acute inflammatory proc- 
ess about the blood- 



THE ]S^EItVOUS SYSTEM. 



757 



known to explain the symptoms. Within the last few years a number 
of cases have been reported in which the lesion was an acute myelitis 
with or without an accompanying polyneuritis (Fig. 447). 

Bailey and Ewing^ reported a case in which the cord showed congestion with capil- 
lary hcemorrhages and circumvascular small round-cell infiltration (Figs. 448 and 449). 
The ganglion cells were in various stages of degeneration. Similar lesions have been 
reported by Marie and Marinesco, by Hertz and Lesne, and by others. Mills and Spiller 
report in some cases a polyneuritis in addition to the myelitis. Krewer finds an acute 
myelitis and neuritis, and considers the lesion due to a non-specific infection. Brault 
reports three cases in which symptoms of Landry's paralysis followed lymphangitic 
abscesses from excoriation of lower limbs. He considers these cases of "myelic locali- 
zation of a streptococcus infection." Remlinger describes a case in Avhich the strepto- 





FiG. 448.— Landry's Paralysis. 

Showing blood-vessels from Fig. 447, more highly 
magnifled. There are congestion and Inflltration of 
the walls with leucocytes. 



Fig. 449.— Landry's Paralysis. 

Showing blood-vessels from Fig. 447, more highly 
magnifled ; leucocytes in the walls. 



COCCUS was detected in the spinal-cord substance by cultivation and by stained sections. 
Remlinger also states that he has induced symptoms of an acute ascending paralysis 
in rabbits by inoculating them with pus from a septic abscess. 



Inflammation of the ^NTebyes. {Neuritis.) 

In the nerves, as in the brain and cord, degenerative changes commonly accompany 
inflammation, and a distinction is often difficult. The difficulty in sharp differentiation 
lies in the fact that degenerative changes in nerves, when intense or long continued, 
often lead to inflammations, and that inflammatory conditions in nerves often determine 
secondary degenerative changes in the nerve fibres. 

Acute Exudative Neuritis. — Acute inflammation of the nerves may oc- 
cur as the result of injury, or it may be secondary to an inflammatory 
process in their vicinity, although, owing to the dense lamellar sheaths 
and the special blood supply, the nerve trunks may escape participation 
in even very severe inflammatory processes in surrounding tissues. The 
inflamed nerve may be red and swollen and infiltrated with serum and 
pus cells. The process may undergo resolution or terminate in destruc- 
tion of the nerve, or it may become chronic and result in the formation 
of new connective tissue. Degeneration and regeneration of the nerve 
fibres, similar to those described as following division of nerve trunks, 
may occur in acute neuritis. 

" Multiple Neuritis " (Degeneration). — While for convenience of refer- 
ence described under its usual title, this lesion is probably always a de- 
generation, and would be properly classified under the head of neurone 
degenerations of toxic origin. It is caused hj the action of certain min- 
' Consult Bailey and Ewing, New York Medical Journal, July, 1896. 



758 THE NEEYOUS SYSTEM. 

eral poisons, for example, alcohol aud lead. It occurs as a complication 
of, or snccedanenm to, certain infectious diseases, for example, diph- 
theria, septicaemia, measles, smallpox, etc. It is sometimes apj)arently 
idiopathic. Changes of a degenerative nature are found in the peripheral 
nerves, and are more marked near the periphery than near the cord. 
Thus the most common nerves affected are the anterior tibial and the 
radial. The most marked changes are in the nerves themselves, there 
being little or no change in the connective tissue. More rarely, espe- 
cially in very acute cases, there are reddening and swelling with some in- 
flammatory reaction in the interstitial tissue. The fibre lesion shows best 
in specimens treated with osmic acid and teased in glycerin (Fig. 450). 
Here the myelin sheath is seen to be broken up, and instead of a contin- 
uous envelope of black stained myelin, the myelin is represented by larger 
or smaller black droplets scattered along a broken or degenerated axis 
cylinder. There may be some increase in the connective tissue. The 




Fig. 450.— Degexeration or Nerte Fibres in Multiple Neuritis. 

From a case of alcohol poisoning. Specimen stained with osmic acid. The broken-down medullary sheath 
and fat droplets are stained deep black. 

sheath of Schwann is usually intact. The muscles supplied by the af- 
fected nerves show various stages of atrophy. The cord and meninges 
usually remain normal. In some cases a spinal meningitis and more or 
less myelitis have been described. 



CHEomo Inflammation of the Brain, Coed, and N^eeyes. 

While this term should be applied only to a primary increase in the 
neuroglia elements at the expense of the parenchymatous, thus making 
the degeneration of the nervous tissue proper entirely secondary, it is 
very difficult always to eliminate the possibility of preceding degenera- 
tive changes. Histologically the lesion consists in a proliferation of the 
neuroglia elements. The neuroglia cells increase in number, some of the 
new- formed cells having many processes, others few. In the early cellu- 
lar stage of its formation the proliferative area is soft and gelatinous, 
and tends to increase the size of the part. With further progress of the 
sclerosis, there is a disproportionate development of fibres attached to 
the cells, and finally of fibres independent of cells. With the increase 
of fibres the affected area becomes firmer, making a sort of dense felt- 
work of interlacing fibrils. In this meshwork are found nerve fibres in 
various stages of degeneration. 

Chronic Interstitial Encephalitis — Sclerosis. — This lesion of the brain 
tissue may occur diffusely, occupying an entire lobe or more or less of the 



THE NERYOUS SYSTEM. 759 

whole brain, or in circumscribed small areas. It consists essentially in 
an increase of the connectiYe -tissue elements, the neuroglia, and an atro- 
phy of the nerYe elements, iDarticularly the ganglion cells and the medul- 
lary sheaths of the nerYes. With these changes are usually associated 
the formation of Gluge's corpuscles, corj)ora amylacea, granular and 
fatty degeneration of the nerve elements, and thickening and x3rolifera- 
tion of cells of the walls of the blood-Ycssels. The areas of sclerosis may 
be Yery dense and hard, or gelatinous in consistence. 

The diffuse form of sclerosis is most frequently seen in general pare- 
sis of the insane, and not infrequently in the brains of drunkards. 

A peculiar feature of disseminated sclerosis is that the patches, 
whether in the brain or cord, do not induce the expected secondary 
degeneration. It is, in fact, uncommon to find secondary degeneration 
resulting from even a large patch of sclerosis. This is belicYcd to be due 
to the fact that in nearly all of the patches the axis cylinders persist even 
after complete destruction of the medullary sheaths. 

The circumscribed form of sclerosis, multiple sclerosis (sclerose en 
plaque), is much* more common than the diffuse form, and may possibly 
occur in the brain alone, or more commonly is associated with a similar 
lesion in the spinal cord. The areas of sclerosis Yary in size from that 
of a j)ea to that of an almond. They may be few or numerous, they may 
be white, grayish, or grayish-red in color, and are usually but not always 
sharply outlined against the unaltered brain tissue. Although in many 
cases the increase in the connectiYC-tissue elements seems to be the pri- 
mary lesion, and the degeneration of the nerve elements secondary to 
this, it is quite possible that in some cases the increase in connective tis- 
sue may be secondary to a degeneration of the nerve elements from loss 
of nutrition or from other causes. 

There is reason for the belief that multiple sclerosis may sometimes be 
the result of disseminated local necrotic lesions of acute infectious dis- 
eases — scarlatina, for examx)le, occurring at an early period of life. ' 

Encephalitis in the New -Born. 

This condition, first described by Virchow, is said to consist in the formation of 
circumscribed collections of cells of various sizes containing many fat granules (granu- 
lar corpuscles) and forming yellowish masses, from 1 mm. to 6 mm. in diameter, in the 
brain tissue. A more diffuse occurrence of granular corpuscles is also described, but 
this is said by some observers to be physiological. The nature of this lesion is but little 
understood, and is still the subject of controversy. 



LESIONS OF THE BRAIN IN GENERAL PARESIS OF THE 

INSANE. 

The changes in this disease are in the main those of chronic diffuse 
encephalitis, but the appearances vary greatly and depend to some extent 
uiDon Y'hether the brain is examined in early or late stages of the disease. 

^ See Op-penlieim, Berl. klin. Wochenschrift, 31arch 2d, 1896. 



760 THE NERVOUS SYSTEM. 

According to Meyer, iu the early stages of the disease the convolutions, 
particularly of the anterior cerebral lobes, are swollen, the gray matter 
is congested and softened in places. The brain tissue is more or less 
infiltrated with leucocytes. Fatty degeneration of the walls of the 
capillaries, and punctate haemorrhages, are also common. 

Ill later stages of the disease a great variety of changes may be ob- 
served: hemorrhagic pachymeningitis, thickening of the dura mater, 
and close adhesions to the skull ; thickening and opacities of the pia 
mater, adhesions of the latter to the dura mater and to the brain tissue. 
The brain tissue is apt to be atrophied, is often very soft, and the ventri- 
cles are dilated and filled with fluid. The pia mater may be cedematous, 
the eiDcndyma thickened and roughened. On microscopical examination 
the neuroglia is found to be increased in amount, the ganglion cells are 
shrunken and sometimes pigmented; the nerve fibres may also be 
atrophied, and the blood-vessels in a condition of fatty or hyaline degen- 
eration. There may be an accumulation of fatty and granular cells along 
the walls of the blood-vessels. Secondary degenerations in the spinal 
cord are not infrequently observed. ' 

Chronic Interstitial Myelitis. — Under this heading are embraced a 
variety of lesions which probably differ from one another somewhat 
in the nature of the changes involved, but more in the seat of the dis- 
ease. We shall consider without special classification the most impor- 
tant forms. 

Chronic Transverse Myelitis. — In certain cases of pressure on the spinal 
cord from a tumor or from displacement of the bones of the vertebral 
column, etc., instead of becoming softened or undergoing acute inflam- 
matory changes, the cord becomes the seat of a localized formation of 
new connective tissue, with consecutive atrophy of more or less of the 
nerve elements in the gray and white matter. The cord becomes in this 
way harder, and sometimes shrunken at the seat of lesion, and gray in 
color. This change may be followed by ascending and descending de- 
generation. 

Chronic Disseminated Myelitis — Multiple Sclerosis. — This lesion, similar 
in its nature to multiple sclerosis of the brain, often occurs with it. It 
consists in the formation, in more or less numerous scattered, circum- 
scribed areas, of new connective tissue, apparently derived from the neu- 
roglia. The formation of new connective tissue is preceded or accom- 
panied by degeneration and atrophy of the nerve fibres and ganglion 
cells. The new connective tissue consists of the characteristic branching 
neuroglia cells, surrounded by a more or less dense network of fine 
fibrillae, many if not most of which seem to be branches of the neuroglia 

^ It is veiy clifflcult to make positive and definite statements regarding many such 
lesions of the brain as those just indicated, or in general of brain lesions wliose nature 
must be revealed by microscopical study, because our technical procedures in the study 
of the brain, even in normal conditions, are still in many respects quite unsatisfactory 
and incomplete. The brain tissue is so delicate and so liable to post-mortem changes, 
and the effects of different preservative agents are so liable to variations, that great 
caution is necessary in arriving at conclusions regarding the more minute lesions affect- 
ing the nerve tissue of the brain. 



THE Is'EEYOUS SYSTEM. 



761 



cells. Cori3ora amylacea and sometimes fat droplets, either free or cod- 
taiued in cells, may be present in the sclerosed areas. 

The areas of sclerosis may involve both gray and white matter, and 
may be very small or large (Fig. 451). If very small or in early stages 
of formation, they may not be recognizable by the naked eye, but when 
visible they are grayish, translucent, and firmer than the surrounding 
tissue, and may or may not present a depressed surface ; they sometimes 
project above the general level. The cause of this as of all other forms 
of so-called idiopathic interstitial myelitis is very obscure. As noted in 
multiple sclerosis in the brain, secondary degenerations are rare, and 
probably for the reason there given. 

Chronic Interstitial Neuritis. — This is essentially a chronic interstitial 
inflammation resulting in an increase of the connective tissue in the nerve 




tNK 



Fig. 451.— Multiple Sclerosis in the Spinal Cord. 

Showing irregular areas in which there are atrophy of the nerve fibres and their replacement by connective 

tissue. 



sheaths and intrafascicular bands. As a result of this the nerve fibres 
undergo atrophy from pressure ; the medullary sheaths and finally the 
axis cylinders being in many of the fibres partially or completely de- 
stroyed. 

Tic Douloureux. — Changes in the peripheral branches of the fifth 
cranial nerve removed from obstinate cases of trifacial neuralgia have 
been reported in a considerable number of cases. These changes consist 
in degeneration of the axis cylinders and of their medullary sheaths. In 
a smaller number of instances changes have been reported in Gasserian 
ganglia removed from such cases. The changes in the ganglia consist in 
atrophy and disappearance of the nerve cells with increase in the con- 
nective-tissue elements. A peculiar shrunken condition of the cell in 
which the cell retracts to one side of its cell space is a fairly character- 
istic feature. But three reports, including in all eight cases, have been 
made upon ganglia examined by Mssl's method. Of these, seven showed 
changes in the chromatic substance. 



762 



THE NERVOUS SYSTEM. 



TUBERCULOUS LESIONS IN THE NERVOUS SYSTEM. 

Tuberculous inflammatiou whether of the braiu or cord is usually sec- 
ondary to tuberculous inflammatiou in other organs, and is most fre- 
quent as an extension of tuberculosis of the meninges. In the brain sub- 
stance it usually manifests itself in the formation of circumscribed masses 
of new tissue from 0.5 to 1 cm. in diameter, or larger. These may be 
single or multiple, are most common in young persons, and very fre- 








>^- 



Fig. 453.— Solitary Tubercle of Cerebellum. 

a, a. Miliary tubercles with griant cells ; h, b, miliary tubercles without giant cells ; c, diffuse tubercle tis- 
sue ; cZ, central cheesy mass e, nerve tissue of the cerebellum. 



quently occur in the cerebellum (Fig. 452). They are apt to occur in 
connection with tuberculous inflammation of other organs. They are 
frequently called solitary tubercles, and usually consist of a dense cen- 
tral cheesy mass, around which is a grayish zone containing tubercle 
granula, numerous small spheroidal cells, with occasionally larger poly- 
hedral cells and giant cells. They do not, as a rule, seem to be formed 
by an aggregation of miliary tubercles, although these may be present 
in the peripherj^ Tubercle bacilli have been found in these solitary 
tubercles. 

They sometimes suppurate and break down, and then they simulate 
simple abscesses. 



THE NERVOUS SYSTEM. 763 

Conglomerate and scattered miliary tubercles of the ordinary form 
sometimes occur in the brain, usually in connection with tuberculous in- 
flammation of the meninges or ependyma. 

In the spinal cord solitary nodules may determine extensive second- 
ary degenerations. Multiple tuberculous foci may occur in the cord. 
They are rare and usually secondary to tuberculosis of the spinal me- 
ninges. 

Tuberculous inflammation of nerves is rare except at their origins, 
where it is due to an extension from tuberculous meninges. When a 
nerve traverses tuberculous tissues, it may be involved in the inflamma- 
tory process. 



SYPHILITIC LESIONS IN THE NERVOUS SYSTEM. 

Syphilitic lesions in the nervous system may occur in either the inher- 
ited or in the acquired form of the disease. In the former it usually 
shows itself early in life, though cases have been reported after puberty. 
Gasne in an examination of twenty-six foetuses of syphilitic parents found 
well-marked syphilitic lesions in four. More commonly it is a tertiary 
manifestation of the acciuired disease occurring from ten to twenty years 
after the initial lesion. Less commonly cerebral symptoms make their 
appearance within a few months after the chancre. The lesion some- 
times appears in the brain as the so-called gummy tumors. These are 
most frequently found near the periphery of the brain, are usually con- 
nected with the meninges, and may be sharply circumscribed. The cen- 
tral portion of the tumor is apt to be in a condition of cheesy degenera- 
tion, and at the periphery is seen fibrous tissue or a dense infiltration of 
small spheroidal cells. 

Syphilitic inflammation of the brain very frequently occurs in a dif- 
fuse form, characterized by the formation of a gelatinous, grayish tissue, 
consisting of a more or less homogeneous or granular basement substance, 
with numerous small round cells. The neighboring nerve elements are 
apt to be atrophied. A most common syphilitic lesion is a specific arte- 
ritis with or without the formation of small gummatous tumors in the 
walls of the vessels. 

Syphilitic inflammation in the cord is usually secondary to a similar 
process in the si^inal meninges. The size and shape of the gummata are 
modified by the restriction of the vertebral canal. The tumors are 
mainly significant from the more or less extensive secondary' degenera- 
tions which they induce. 

The relation of syphilis to multiple cerebral and spinal sclerosis is 
still uncertain. Its relation to tabes and to dementia paralytica has been 
noted under their respective titles. It is probable that most or all of 
those rare cases of tabes occurring in children are the results of inherited 
syphilis. 

Syphilitic inflammation of the peripheral nerves is, like tuberculous 



764 THE NEEYOUS SYSTEM. 

inflammation of nerYes, usually dependent upon an extension of the 
process either from the meninges or from some tissue through which the 
nerYes pass. 

ACTINOMYCOSIS. 

Actinomycosis of the brain has been described. It is a rare form of 
brain infection, and is usually secondary to actinomycosis of the neck or 
face. The condition is apt to lead to suppuration and abscess formation. 
A case has been reported by Bollinger in which the disease was appar- 
ently iDrimary in the brain. 

LEPROUS INFLAMMATION. 

This occurs in the peripheral nerYes and consists in the formation 
within the nerYes of masses of new-formed tissue somewhat resembling 
granulation tissue. In the cells of this tissue multitudes of characteristic 
bacilli are uniformly found (see Leprosy). It constitutes the Yariety of 
leprosy known as lej)ra ansesthetica. 

TUMORS. 

Tumors occurring in the nerYOus system may be of the types found 
in the other organs or of types peculiar to nerYOus tissue. They may be 
primary, or secondary to similar growths in other parts of the body. 

Tumors of the Brain. 

Myxoma, fibroma, lipoma, and osteoma are rare forms of brain tumor. 

Neuroglioma Ganglionare. — This is a form of tumor probably due to 
disturbances in the dcYelopment of the brain. It is peculiar to nerYOUS 
tissue and occurs in the form of circumscribed tumors or of diffuse en- 
largements of portions of the brain. The pia mater OYcr these tumors 
is unchanged and the couYolutions retain their shape. The tumors are 
formed of neuroglia, in which are contained little groups of ganglion 
cells (Ziegler). 

Glioma. — This is the most common tumor of the brain, and like the 
preceding is found only in the nerYOus system. It occurs with especial 
frequency in children and young adults. Such tumors occur in all 
parts of the brain, but they are found most frequently in the cerebrum. 
There may be a single tumor, or there may be scYcral such tumors in 
different parts of the brain ; some of them attain a large size. Bramwell 
reports a case in which considerably more than one-half of a hemisphere 
was iuYolYcd. These tumors may be sharply circumscribed, or merge 
imperceptibly into the brain substance ; sometimes the tumor is arranged 
so as to form the wall of a cyst which contains clear serum. They may 



THE XEEYOUS SYSTEM. 765 

be white and hard; gray, soft, and gelatinous; infiltrated with small 
haemorrhages or partly degenerated and softened. The centre of a gli- 
oma maj' break down and become soft and necrotic or even fluid. In 
this way a cyst is formed having a wall of gliomatous tissue. The brain 
tissue around these tumors may be inflamed or necrotic. These tumors 
arise from the neuroglia. The relative quantity of cells and fibrils varies 
in different tumors. They are composed of neuroglia cell^ and their 
delicate interlacing processes (for minute structure see ^' Glioma^'). If 
the tissue is of a loose formation with wide meshes between the fibres it 
presents a myxomatous appearance, and has been described as myxo- 
giioma. When the cellular elements are very numerous the tumor is 
often referred to as a glio-sarcoma. In some cases the vascularity' is such 
a marked feature that the name of telangiectatic glioma is applied to it. 
(According to Ziegler, a simple preponderance of cells, so long as they 
are of the neuroglia \jj)e, does not warrant classing the tumor as a sar- 
coma, and he Insists that the latter term should be reserved for those 
gliomata in which an active proliferation of the connective tissue of the 
walls of the blood-vessels occurs. ) Osier reports three out of five cases 
of gliomata as made up of large cells in contradistinction to the small - 
cell variety. 

Sarcoma occurs in any part of the brain. It may be single or multi- 
ple. The tumors are composed of round or fusiform cells with more or 
less basement substance. 

Endothelioma is found in the substance of the brain. The tumors are 
of the types described as occurring in the x)ia mater. 

Angioma. — Small collections of dilated vessels are found in the sub- 
stance of the brain. They seem to be congenital like the nsevi of the 
skin. 

Carcinoma occurs in the brain. It is usually, if not always, secon- 
dary to carcinoma in some other organ. 



TU]\IOES OF THE COED. 

In the pia mater of the cord are sometimes found small fibromata, 
osteomata, and lipomata. Multiple fibromata occasionally occur in the 
cord in connection with multiple fibromata of the peripheral nerves. 

Endotheliomata of the types described as existing in the pia mater of 
the brain are much more rarely found in the pia mater of the cord. 

A fatty sarcoma' of the pia mater, which infiltrated the cord, formed 
a tumor as large as a filbert, and had for twelve years caused gradually 
increasing paraplegia, has been described. 

Two curious cases^ of diffuse sarcoma and one of endothelioma of the 
pia mater of the whole length of the cord are recorded. They occurred 
in girls of four-and-a-half, sixteen, and twenty-two years of age. In each 

1 Turner. Trans. London Path. Soc, xxxix. 

2 Conpland, Trans. London Path. Soc, xxxviii. ; Arch, fiir Psych., 1885. 



766 THE NERVOUS SYSTEM. 

case the pia mater of the whole length of the cord was diffusely thickened 
and studded with nodules. In two of the cases the growth was com- 
posed of round cells, in the third case of large endothelial cells arranged 
in alveoli. In two of the cases the clinical symptoms lasted only for 
about three weeks, in the third case for five months. The acuteness 
of the symptoms was such as to indicate the existence of spinal menin- 
gitis. 

In the si)inal cord itself gliomata, fibromata, sarcomata, glio-sarcomata, 
and angio-sarcomata occur, but are rare. 

When gliomata or glio-sarcomata do occur in the spinal cord, the new 
growth is apt to extend for some distance lengthwise in the cord and to 
be attended with the formation of a cavity ; this condition is usually de- 
scribed under the name of syringomyelia. 

Cysts may occur as a result of softening or from unknown causes. 
Sometimes very long, narrow canals are found in the spinal cord, even 
reaching nearly its whole length. Some of these are evidently the di- 
lated central canal, as they are lined with epithelium. Others, how- 
ever, doubtless originate in haemorrhages (see Hsematomyelopore, page 
727). 

Syringomyelia. — This lesion of the spinal cord consists in the formation 
of gliomatous or glio-sarcomatous tissue in the vicinity of the central canal, 
and its subsequent partial disintegration with the formation of one or more 



S!vSc;o, ii 



-y^ 






^ 






Fig. 453.— Syringomyelia. 
An Irregular cavity in the gray matter of the spinal cord, lined by a thick layer of gliomatous tissue. 

cavities within the substance of the cord (Fig. 453). These cavities, 
which are filled with fluid, vary greatly in size, shape, and extent, and, 
while usually situated in the central region of the cord, may involve the 
anterior and posterior cornua and invade the posterior columns. There 
may be two communicating cavities, and these may, but usually do not, 
open into the central canal. The longitudinal extent of these cavities 
varies greatly. The lower cervical and upper dorsal regions are most 
frequently involved. The cavity is usually lined with tissue somewhat 
denser than that which makes up the bulk of the tumor. The gliomatous 



THE NERVOUS SYSTEM. 767 

or glio-sarcomatons tissue which forms the basis of the lesion in syringo- 
myelia i^robably originates from the layer of nenrogiia which snrronnds 
or extends away from the central canal. 

Syringomyelia is freqnently mistaken for hydromyelia which is a 
congenital malformation, and in which the longitudinal cavity in the 
cord is at some period lined with epithelial cells. Syringomyelia has 
also been confused with hgematomyelopore. 

There seems, furthermore, to be a class of lesions of the cord, usually 
classed as syringomyelia, in which cavities of various forms coexist with 
a tumor in the vicinity of the central canal. But these cavities do not 
appear to be formed by a breaking down of the tumor tissue, but in some 
other way as yet little understood. 

Tumors of Keryes. 

The tumors of the nerves may be divided into those consisting largely 
of or containing new-formed nerve tissue — true neuromata, and the so- 
called false neuromata, which are for the most part fibromata or myxo- 
mata originating in the connective tissue of the nerve (see I^euroma). 
Myxo-sarcomata are less common, and primary sarcomata rare. The 
nerves may be secondarily involved in sarcomata or in carcinomata 
through which they pass, though not infrequently nerves pass through 
these tumors without being in the least involved in their peculiar struc- 
ture. Paltauf has described as endotheliomata rare tumors of the glan- 
dula carotica. 

PARASITES. 

Cysticercus and more rarely echinococcus occur in the brain. 



HOLES AND CYSTS IN THE BRAIN. 

Larger or smaller holes may be found in the brain tissue from dilata- 
tion of the perivascular lymph-spaces, or well-formed cysts may exist 
as a result of hsemorrhage, inflammatory softening, hydatids, etc. 



Porencephalus 

is a term which has had a wide range of application to various defects of 
the brain substance. By some writers the term has been used to cover 
almost any congenital absence of brain tissue. By others brain defects not 
congenital are included. Its most common application is to certain quite 
well-defined congenital conditions in which there is an absence of a con- 
siderable portion of one or both hemispheres. These holes may lie deep 
in the substance of the brain. More commonly they come to the surface 
making conical depressions in the cortex, which the dura mater bridges 



768 THE NERVOUS SYSTEM. 

over, but into which the pia extends. There may or may not be commu- 
nication with the ventricles. This condition may coexist with various 
mental aberrations, hydrocephalus, etc. Similar defects may occur in 
the cerebellum. 

Pineal Gland. 

This little body, about the size of a cherry stone, is composed of con- 
nective tissue enclosing cavities, which are filled with reticulated tissue 
and round cells. The cavities often contain brain sand. 

A small number of tumors belonging to the class of teratoma have 
been described as originating in the pineal gland. 

Weigert ' describes a tumor, about 3. 5 cm. in diameter, composed of 
epidermis, hair follicles, hair, sebaceous glands, cartilage, fat, smooth 
muscle, and cylindrical epithelium. 

Falkson^ describes a chondro-cysto-sarcoma, 5.8 cm. in diameter, 
which apx)arently originated in the pineal gland. 

Turner^ describes a tumor of the pineal gland, projecting into the 
third ventricle and the left lateral ventricle, of the size of a kidney. The 
tumor was composed of fusiform cells, of nerve ganglion cells, of tubules 
and acini lined with cylindrical epithelium, and of more irregular spaces 
filled with large polygonal cells. 

Coats^ describes a tumor, three inches in diameter, growing into the 
third ventricle, the aqueduct of Sylvius, and the fourth ventricle. It 
was composed of fusiform cells, of tubules lined with cylindrical eiDi- 
thelium, of irregular masses of epithelium, of cartilage, and of smooth 
muscle. 

Hypertrophy with cystic degeneration may occur. 

Haemorrhage into the substance of the gland has been described. 



Hypophysis Cerebri (The Pituitary Body.) 

This structure consists of two lobes ; the anterior lobe is composed of 
a connective -tissue stroma enclosing cavities which are packed full of 
nucleated cells of various sizes and shapes, some of them resembling 
nerve cells ; the posterior lobe is com^DOsed of vascular connective tissue. 

Tumors. — Weigert ^ describes a tumor, as large as a hen's egg, which 
resembled in its structure the normal anterior lobe of the pituitary body, 
and which he regards as a hypertrophy of that body. Weigert also de- 
scribes a gummy tumor of the pituitary body as large as a hazelnut. 
Weichselbaum describes an adenoma of the iDituitary body as large as a 
pigeon's egg, closely resembling the structure of the normal anterior lobe 
of this body ; a small lipoma ; and a pituitary body with colloid cysts, 
lined with ciliated epithelium. 

iVirch. Arch., Ixv., ip. 212. ^jbid., Ixxv., p. 550. 

'^ Trans. London Path. Soc, xxxvi. ■*Ibid., xxxviii. 

syii-f.!, ^j-ch ixv., p. 219. 



THE N^ERYOUS SYSTEM. 769 



Methods of Preparation of Nerve Tissue for Microscopical Study. 

The general methods of liardening have ah'eady been given on pages 16 and 19. 
For minute study there is no one method of staining and mounting upon which we can 
rely exclusively for the study of all lesions. A preliminary examination of areas of 
inflammatory softening, or of the disintegrated tissue in ajioplectic clots, or of the new- 
fo]-med tissue in chronic Imrnorrliagic pachymeningitis interna, may be made by teasing 
portions of the affected tissues in one-half-per-cent salt solution. Or the tissues in 
these lesions, or in any others in which fatty degeneration is suspected, may be placed 
for twenty-four hours in one-per-cent aqueous solution of osmic acid, and then washed 
and teased in glycerin. In this way the myelin and the fat will be stained brown or 
black. Secondary and other degenerations of medullated nerves may be studied by 
soaking the nerves for tAventy-four hours in one-per-cent solution of osmic acid, and 
then staining Avith picrocarmine and teasing and mounting in glycerin. 

To demonstrate the presence of miliary aneurisms in or about apoplectic clots, it 
is usually necessary to macerate the brain tissue in water until the nerve elements dis- 
integrate, and they may then be washed away under a stream of water, leaving the 
blood-vessels with their aneurisms exposed. 

MarchVs Method. — For studying early stages of degeneration in medullated nerve 
fibres this method is invaluable. It depends upon the fact that while myelin and fat 
both stain black, when the fresh nerve fibres are placed directly into osmic acid, a pre- 
liminary soaking in a solution of potassium bichromate so affects the tissue that the 
myelin sheaths of normal fibres no longer impregnate with osmiun, the fat droplets 
alone staining. 

Tissues are first hardened from one to three weeks in Miiller's fluid, or simply in a 
two or three per cent aqueous solution of potassium bichromate. They are then 
transferred to a mixture of one-per-cent aqueous solution of osmic acid one part, 
Miiller's fluid two parts, where they remain from three days to a w^eek. 

By following the lines of fat droplets, degenerative changes in nerve fibres may be 
traced either in the peripheral nerves or in the central nervous S3"stem. 

Eosin-Rmnatoxylin Staining. — Suppurative inflammation of the central nervous 
system and its membranes, or the connective-tissue changes in general, may be studied 
in sections from the tissues hardened in Miiller's fluid and alcohol, stained double with 
hsematoxylin and eosin (see page 59), and mounted in Canada balsam. 

Weigerfs Method. — A very useful method of staining sections of nerve tissue, espe- 
cially of the brain and cord, is that known as Weigert's hcematoxylin method. The tissue 
is first Avell hardened in Miiller's fluid. 

Blocks of the hardened tissue are embedded in celloidin and sections made in the 
usual way. The sections are first soaked for twenty-four hours in a saturated aqueous 
solution of neutral cupric acetate diluted with an equal bulk of water, or, if the material 
has been kept some time and takes the haematoxylin stain with difficulty, a better result 
is often obtained by soaking the sections for from twelve to twenty-four liours in a three 
to five per cent aqueous solution of bichromate of copper before staining. They are 
now thoroughly washed twice in water, then in alcohol, and then are transferred to the 
haematoxjdin solution, made as follows: 

Hsematoxylin crystals 1 gm. 

Alcohol, 97 per cent 10 c.c. 

Water 90 " 

Saturated aqueous solution lithium carbonate 1 " 

In this solution the sections remain for two hours. (If the finer fibres of the cere- 
bral cortex are to be brought out the sections must remain for twenty-four hours in the 
haematoxylin solution.) The sections are now thoroughly washed in two or three 
waters and transferred to the bleaching solution, composed as follows : 

Potassium ferricyanide 2.5 gm. 

Sodium biborate 2. " 

Water 200 c.c. 

49 



770 THE NERVOUS SYSTEM. 

In this fluid the sections discharge a brownish color, and they remain in it until the 
gray matter has a distinct yellow color and the white matter is bluish-black. The 
time required to produce this efiiect varies considerably, and is usually from half an 
hour to an hour. The sections are now washed, dehydrated with alcohol, cleared up in 
oil of cloves or oil of origanum, and mounted in balsam. The sections may be stained in 
alum carmine before dehydration, to bring put the nuclei. In sections stained by this 
method the gray matter, connective-tissue elements, and ganglion cells have a yellow 
or yellowish -brown color, the axis cylinders are uncolored or have slight yellowish tint, 
while the medullary sheaths are bluish-black or black. 

JS^issl's Staining Metlwd. — There are several variations of this method, but the fol-. 
lowing gives good results in most cases : 

The essential feature of the so-called Nissl's method is the application of the aniline 
dyes to the staining of certain structural elements in the nucleus and cytoplasm, which 
are distinguished from the other structures of the cell by a differentiating decoloriza- 
tion with alcohol. 

Methylene blue is the most generally useful of the aniline dyes for this purpose. 

The specimens should have been carefully hardened in sublimate solution or in 
alcohol or in formalin. 

Very thin sections are stained in one-per-cent solution of methylene blue. The 
staining may be effected on a slide on which the sections are floating in the blue solu- 
tion by gently heatiug over a lamp until the fluid steams. 

The sections are now transferred to a mixture of absolute alcohol 90 parts, 
with aniline oil 10 parts, in which the differentiation is effected by the use of successive 
fresh portions of fluid until slight but distinct differentiation in color is seen between 
the gray and white matter of the nerve tissue. The exact degree of decolorization 
which gives the best pictures will be learned by practice of the method. In many cases 
the use of alcohol alone without aniline oil is preferable to the mixture, and in any case 
the sections should always be washed in strong, pure alcohol before passing on to the 
xylol. The sections are now freed from the bulk of the alcohol upon the slide, cleared 
in xylol, and mounted in dammar varnish, in which the color is apt to be preserved 
better than in balsam. By this procedure the chromophilic bodies in the cytoplasm of 
ganglion cells are sharplj^ differentiated, and thus abnormal conditions may be detected 
in them (see Plate XIII. ). 

A contrast stain with erythrosin (Held') is useful in demonstrating cell structures 
which are not visible with the simple Nissl staining. This may be secured as follows : 

The sections are first warmed from one to two minutes in the following solution : 
erythrosin, gm. 1; acetone, gtt. ij. ; aqua dest., 150 c.c. They are then washed thor- 
oughly in water and transferred to a solution consisting of equal parts of Nissl's methy- 
lene blue solution and a five-per-cent aqueous solution of acetone. In this they are 
warmed until the odor of acetone ceases to be given off. The sections are decolorized 
in a one-tenth -per-cent solution of alum until they appear red in color, and are then de- 
hydrated in alcohol and cleared and mounted in the usual way. 

, 'Held, Arch. f. Anat. und Phys., anat. Abt., 1895, p. 396; 1897, p. 204. 



INDEX. 



Abbott, Principles of Bacteriology, ref. 152 
Abdomen, post-mortem changes in, 20 

post-mortem examination of, 19, 27, 42 
Abdominal pregnancy, 640 

viscera, position of, 20 

viscera, sudden death after lesions of, 
50 
Ahel and Davis, on skin pigment, ref. 88 
Ahrainow, ref. blood-vessel changes in 
syphilis, 233 ; peritonitis, 523 ; syphilitic 
lesions of blood-vessels, 418 
Abrin in toxaemia, ref. Flexner, 178 

toxic action of, 161, 827 
Abscess, 177 

embolic, 115 

metastatic, 180 

of bone, 668 

of brain, 718, 752 

of Cowper's glands, 659 

of heart, 403 

of kidney, 571 

of liver, 114, 544 

of lung, 457 

of mamma, 641 

of muscle, 692 

of prostate. 658 

of spleen, 376 

of testicle, 653 

repair of, 1 20 
Acarus scabiei, 139 
Acliardand Phulpin. post-mortem invasion 

by bacteria, ref. 166 
Achorion Schonleinii, 157 
Achromatic figure in mitosis, 96 

substance in nerve cells, 731 
Acid, arsenious, 323 

carbolic, 145, 326 

carbonic, 328 

hj'drochloric, 322 

hvdrocvanic, 326 

nitric, 321 

oxalic, 322 

sulphuric, 321 

tartaric, 322 
Aconite, poisonous effects of, 328 
Acrania, 715 
Acromegalia. 336 
Actinomvces, 201 

bovis. 200 

group of organisms, 201 
Actinomycosis. 199. 764 
Adami, definition of inflammation, ref. 126 

ref. on bacteria in blood, 181 

on germicidal action of liver, 551 

on inflammation and fibrosis, 122 



Adami on latent infection and sub-infec- 
tion, 160 

on retroperitoneal lipoma, 524 

on reversion, 549 

on tumors, 272 
xVdaptation in pathological processes, ref. 

Welch, 127 
Addison's disease, 332 

autotoxic nature of, 330 

internal secretion, changes of. in, 383 

pigment in, 88 
Adenie. 360 

Adenoid polyps of pharynx, 489 
" Adenoids "'^( see Pharyngitis), 488 
Adeno-carcinoma, 307 

of stomach, 502 

of uterus, 621 
Adeno-cystoma of mamma, 645 

of ov^aries, 682 
Adeno -sarcoma, 2{)1 

of dura mater spinalis, 709 
Adenoma, 307 

of adrenals, 886 

of bronchi, 442 

of gall ducts, 562 

of intestine. 519 

of kidney. 590 

of liver, 555 

of lung. 480 

of mamma, 645 

of mouth. 484 

of oesophagus, 492 

of ovaries, 682 

of prostate, 659 

of stomach, 501 

of testicles, 656 

of uterus, 619 
Adler, ref. on diagnosis of malignant 
tumors of the lungs, 480 ; cardiac syph- 
ilis, 406 ; forms of emigrated leucocytes, 
111 ^ 

Adler and Meltzer on "tissue spaces," 426 
Adrenal extract, effects of, on body, bibli- 
ography, ref. Bates, 388 
Adrenals,* 385 

accessory, 885 

Addison's disease, relation of, to, 882 

degenerations of. 385 

examination post mortem of, 28, 43 

extirpation of, ref. Tizzoni, 388 

formation of. period of, 39 

hfiemorrhage of. 385 

hardening of, 29 

hyperplasia of, 886 

inflammation of, 885 



772 



INDEX. 



Adrenals, malformations of, 385 

pigmentation of, 385 

post-mortem changes in, 29 

shape of, 28 

situation of, 28 

size of, 29 

structure of, 29 

syphilis of, 386 

thrombosis of, 385 

tuberculosis of, 385 

weight of, 29 
Aerobic bacteria, 144 
Afanassieff, on granulation tissue and 

infection, ref. 160 
Agar as culture medium, 152 
Agglutination in cholera bacillus, 214 

of red blood cells, 214 

of typhoid bacillus, 213 
Ague (see Malaria), 252 
Ague-cake (see Spleen), 377 
Aguillula, 138 

ATilfeldt on placental cysts, ref. 628 
Air, bacteria in, 147 

emboli, 354 

in blood, 354 

in pericardium, 387 

in pleura, 483 

micro-organisms in, ref. to GotUtein, 
159 

passages, condition of, after drown- 
ing, 47 
Albumin film for fixing paraffin sections 
to slide, 57 

mixture for fixing sections to slide, 
52 
Albuminous degeneration, 79 

degeneration, restoration of cells after, 
99 
Albuminuria, 566 
Alcohol, poisonous effects of, 326 

use of, in fixation of tissue, 52 
Alexander on relations of adrenals to ner- 
vous system, ref. 385 
Alexines, 125, 169 

Alkaloidal poisons in putrefaction, 328 
Aloes, poisonous effects of, 325 
Alveolar sarcoma, 289 
Amoeba coli, 128 

dysenterica, 128 

phagoc3"tic powers of, 124 

response of, to injury, 124 
Amoebic dysentery, 511 
Amoeboid bodies in malaria, 252 

movement of leucocytes in inflamma- 
tion, 109 
Amitosis, 97 

in epithelium, 102 
Ammonia, poisonous action of, 322 
Amsperger on origin of dermoid cysts of 

ovary, ref. 637 
Amyelia, 716 
Amyloid degeneration, 82 

degeneration, common seats of, 83 

degeneration, experimental, 83 

tests for, 28, 83 

tumors of larynx and trachea, 432 

tumors of tongue, 485 



Amyotrophic lateral sclerosis, 745 
Anaemia, 69, 343 

atypical forms of, 358 

blood changes in, 345 

bone changes in, 677 

infantile, 361 

of brain, 721 

of kidney, 565 

of liver, 535 

of lungs, 443 

pernicious, 344, 356 

secondary, 344, 356 
Anaerobic bacteria, 144 
Anders on pancreatic haemorrhage, ref. 

532 
Anencephalia, 715 
Aneurism, 418 

cirsoid, 419 

cylindrical, 418 

dissecting, 419, 420 

fusiform, 418 

miliary, 421, 723 

of aorta. 420 

of arteries, formation of, in arterio- 
sclerosis, 415 

of brain, miliary, 723 

of cerebral arteries, 723 

of coronary arteries, 420 

of heart, 397 

of pulmonary arteries, 420 ■ 

of splenic artery, 372 

sacculated, 418 

varicose, 419 
Aneurismal varix, 419 
Angina (see Pharyngitis), 487 

membranous, 186 
Angioma, 301 

cavernosum, 303 

of bone, 681 

of brain, 765 

of choroid plexus, 714 

of ependyma, 714 

of goitre, 383 

of kidney, 590 

of larynx, 432 

of liver, 554 

of mouth, 484 

of penis, 651 

of spleen, 380 

of tongue, 485 

of uterus, 619 

simplex, 303 

telangiectoides, 303 
Angio-sarcoma, 289 

of liver, 556 
Anhydraemia, 342 
Anilin dyes as bacterial stains, 149 

gentian violet solution in Gram's stain, 
150 
Animal parasites, 128 
Animals, infectious diseases of, 260 
Ankylostoma duodenalis, 136 
Anopheles, 255 
Anthracosis of lungs, 462 

of lymph-nodes, 363 
Anthrax, 197 

bacillus, characters of, 198 



INDEX. 



773 



Anthrax of intestine, 508 

Antitoxic serum, Ij^sogenic action of. 216 

substances, nature of, 171 
Antitoxin. 171 

of diphtheria. 172, 238 

of plague, 243 

of pneumonia. 191 

of tetanus. 240 

streptococcus, 185 
Anus, atresia of, 503 
Aorta, aneurisms of 420 

atheroma of, 414 

double, dissecting aneurism simulat- 
ing, 420 

examination of, 33 « 

hypoplasia of, 337, 338 

inflammation of, 414 

malformations of, 390 

obliteration of, 421 

stenosis of, 421 
Aphthae, 158, 485 
Apoplexy of brain, 722 

of placenta, 627 

of spinal cord, 725 

serous, 722 
Appendicitis, 517 

bibliography of, ref. 518 

excitants of, 518 

tuberculous, 517 
Appendix, concretions of, 517 

foreign bodies in, 517 

gangrene of, 517 

inflammation of (see Appendicitis). 
517 

necrosis of, 517 

strictures of, 517 

tuberculosis of, 517 

tumors of. 520 
Arachnoid, 699 
Argyria, 88 

Am and on adrenal haemorrhage, ref. 385 
Arnold, ref. angiosarcoma of liver, 556; 
on fibrin formation, 112; on hairy pol^q^s 
of pharynx, 489 ; iron pigment in cells, 
462 ; lymph-nodules in viscera, 362 
Arsenic, compounds of, poisonous effects 
of, 324 

poisoning bv, post-mortem examina- 
tions in, 38, 324 

poisonous action of, 323 
Artefacts of the nervous system, 17, 754 
Arteries, aneurisms of, 415, 418 , 

atheroma of, 413 

calcification of, 411 

cerebral, lesions of, 730 

chronic inflammation, conditions lead- 
ing to, 416 

chronic inflammation of (see Arterio- 
sclerosis), 412 

coronary, anastomoses of, 404 

coronar}^ aneurisms of, 420 

coronar}^ distribution of, 404 

coronary, embolism of, 403 

coronary, examination of, 24 

coronary, thrombosis of, 402 

degeneration of, 82, 411 

fibrous nodules in pericardium, 390 



Arteries, hepatic lesions of, 537 

inflammation of (see Arteritis), 412 

pulmonary, aneurisms of, 420 

pulmonary, embolism of, 445 

pulmonary, malformations of, 390 

pulmonary, thrombosis of, 445 

rupture of, 410 

sclerosis of, 412 

structure of, in hsematophilia, 71 

syphilitic inflammation of, 417 

terminal arteries, emboli in, 76 

tuberculous inflammation of, 417 

tumors of, 421 

wounds of, 410 
Arterio-sclerosis (see Arteritis), 412 

classification of forms of, 416 

conditions leading to, 416 

relation of, to nephritis, 585 
Arteritis, 412 

peri-, nodosa, 416 

sj'philitic, 417 

tuberculous, 417 
Artery, renal, embolism of, 565 

renal, thrombosis of, 565 

splenic, aneurism of, 372 i 

Arthritis, 682 

chronic, 683 

deformans, 683 

exudative, 682 

gonococcal, 683 

gouty, 684 

pneumococcic, ref. Gave, 683 

rheumatic, 683 

sero-fibrinous, 682 

suppurative, 682 

tuberculous, 684 

uritica, 684 
Arthropathy, hypertrophic, pulmonary, 

336 
Arthropods, 139 
Arthrospores in bacteria, 144 
Ascaris, 135 

in bladder, urinary, 598 

in liver, 559 

in pancreas, 533 
Asclioff, ref. to, on compensatory hyper- 
trophy, 93, 106; on cysts. 278; on decid- 
uoma, 626; on parenchyma cell emboli, 
75; on tumors, 273, 319 
Ascites, 521 

chylous, 426 
Ascospores, 156 
Asiatic cholera, 214 

cholera, lysogenic action of antitoxic 
serum of, 216 
Asphyxia, 44 

in drowning, 46 
Ataxia, cerebellar, 751 

Friedreich's, 751 

hereditary, 751 

locomotor, 745 
Atelectasis, pulmonary, 446 
Atelomyelia, 716 
Atheroma of aorta, 414 

of arteries, 413 
Atresia ani, 503 
Atrophia musculorum lipomatosa, 689 



774 



INDEX. 



Atrophy, 78 

acute yellow, of liver, 539 

brown, of heart, 394 

brown, pigment in, 88 

degenerative, 79 

of adrenals, 385 

of blood-vessels, 410 

of bones, 661 

of brain, 719 

of fat, pericardial, 394 

of glomeruli of kidney, 578 

of heart, 394 

of kidney, 582 

of liver, 539 

of lymph-nodes, 363 

of muscle, 687 

of pancreas, 529 

of prostate, 657 

of spleen, 372 

of stomach, 494 

of testicle, 653 

of thymus, 381 

of thyroid, 382 

of uterus, 610 

progressive, of muscle, 687, 689 

simple, 79 
Auerbach, ref. on typhoid bacilli in blood, 

212 
Avfrecht, ref. on experimental pneumonia, 

459 
Auto-intoxication, 162, 328, 329 

acromegalia as an, 337 

Addison's disease as an, 332 

burns as excitants of, 49 

cachexia strumipriva as an, 331 

diabetes as an, 334 

dyscrasic, 330 

enterogenic, 329 

exophthalmic goitre as an, 332 

gout as an, 335 

myxoedema as an, 331 

nature of, 320 

retention, 329 

scorbutus as an, 336 

sunstroke as an, 335 
Autonomy of tumors, 262 
Autopsies, making of, 3 

medico-legal, 37, 38, 39 
Axis-cylinder process, nature of, 730 
Axone, 732 

changes in, from separation from its 
cell body, 735 

nature of, 730 

Babes, ref. on bacteria and putrefaction in 
dead bodies, 5; on haemorrhagic septi- 
caemia, 243 
Bacilli (see Bacillus), 141 
Bacillus, 141 

aerogenes capsulatus, 243 

anthracis, 198 

branching forms, 142 

coli communis, 187 

conjunctivitidis, 203 

dipiitherige, 235 

diphtherige, branching forms, 237 

diphtlieriae, group resembling, 239 



Bacillus diphtherige, varieties of, 239 

gas, 243 

growth forms, 142 

hsemorrhagicus, 243 

hsemorrhagicus, group of, 244 

hcemorrhagicus septicus, 243 

hoemorrhagicus velenosus, 243 

hay, 229 

icteroides, 248 

influenzae, 202 

lepra, 231 

Lustgarten's, 232 

mallei, 195 

oedematis maligni, 244 

plague, 242 

pneiunouige, Friedlander, 189 

pseudo-diphtherige, 239 

pseudo-intluenzge, 203 

pseudo-tetanicus, 240 

pseudo-tuberculosis, 197 

pyocyaneus, 188 

rhinoscleromatis, 235 

smegma, 229 

syphilis, 232 

tetani, 239 

thread forms of, 142 

tuberculosis, action of, in body, 217 

tuberculosis, avian, 225 

tuberculosis, branching forms of, 222 

tuberculosis, characters of, 222 

tuberculosis, cultivation of, 223 

tuberculosis, dead, action of, 225 

tuberculosis, distribution in body, 227 

tuberculosis, mammalian, 225 

tuberculosis, numbers of, in lesions, 
227 

tuberculosis, portals of entry of, 228 

tuberculosis, pyogenic action of, 222 

tuberculosis, sources of, 228 

tuberculosis, staining methods for, 
223, 224, 225 

tuberculosis, varieties of, 225 

tuberculosis, virulence variable in, 
368; ref. Lartigau 

typhosus, 203 

typhosus, action and characters of, 204 

Welchii, 243 
Bacteria, 140 

action of cold on, 144 

action of disinfectants on, 145 

action of germicides on, 145 

action of heat on, 144 

action of, in body, 160 

action of, in cells, 61 

action of, in fermentation, 146 

action of, in putrefaction, 146 

action of light on, 145 

action of sublimate on, 145 

aerobic, 144 

aerogenic, 146 

agglutination of, 213 

anaerobic, 144 

anaerobic cultures of, 154 

as commensals, 148 

as excitants of inflammation, 161 

as messmates, 148 

biology of, 144 



INDEX. 



775 



Bacteria, branching, 142 
capsules of, 140 
chromogcnic, 146 
classitication of, 148 
Clostridium forms of, 141 
collection of material containing, 

155 
colonies of, 152 
conditions of life of, 144 
conveyance of, by insects, 160 
cultivation of, 151 
degeneration of, 141 
destruction of, by phagocytes, 124 
destruction of, in body, 160 • 
development of, from spores, 143 
distribution of, 145, 146 
elimination of, from body, 160 
entrance of, through gastro-intestinal 

canal, 160 
environment, influence of, 143 
enz3axie producing, 144, 146 
excitation of tumors by, 270 
ferments formed by, 146 
filamentous forms, 142 
fission in, 141 
flagella of, 140 
food of, 144 
forms of, 146 

freezing, effects of, on, 144 
functions of, 144 
function, specialization of, 142 
gas-producing, 146 
genera in, 149 

granules, metachromatic in, 141 
grouping of, 142 

groups of, as disease excitants, 175 ' 
growth, aggregates of, 142 
harmlessness of certain forms in body, 

159 
higher forms, 142 
in air, 147 

in blood in septicaemia, 181 
in dust, 147 
in endocarditis, 407 
infectious diseases incited by, 174 
in heart emboli, 404 
in lungs, 459 ; ref . Beco 
in mouth, 485 

in nose, 429; ref. to Hoicard 
in pseudo-membranous inflammation, 

189 
intestinal, ref., 514 
involution forms of, 141 
in water, 147 
local vulnerability of tissue to action 

of, 160 
membranes of, 140 
metabolic products of, 146 
metabolism of, 145 
methods of study of, 149 
modes of entrance to body, 160 
monomorphism in. 143 
morphology of, 140 
multiplication of, 141 
necrotizing action of, 161 
nomenclature of, 149 
nuclei in, 140 



Bacteria, numbers of, as influencing infec- 
tion, 163 

nutrition of, 144 

occurrence of, in the body, 159 

optical means for study of, 151 

parasitic, 147 

pathogenic, 146, 165 

pathogenic, mode of action of, 168 

photogenic, 146 

physiolog}^ of, 144 

plate cultures of, 152 

pleomorphism in, 143 

polymorphous, 142 

portals of entry of, intestinal canal, 
523 

post-mortem invasion by, 166 

proofs of infective nature, 162 

ptomain poisoning, 146 

pyogenic, 176, 181 

races of, 149 

racket-shaped, 141 

relation of granulation tissue to, ref. 
160 

relation of, to chemotaxis, 145 

relation of, to disease, 159 

relation of, to moisture, 144 

relation of, to nitrogen, 144 

relation of, to other plants and to ani- 
mals, 147 

relation of, to oxygen, 144 

relation of, to putrefactive changes in 
dead bodies, 5 

relation of, to temperature, 144 

reproduction of, by division, 141 

rod-like, 141 

role of, in nature, 145 

safeguards of the body against, 159 

saprophytic, 147 

significance of, in air, soil, and water, 
147 

significance of, in body, 162 

species in, 148, 149 

spheroidal, 140 

spiral, 141, 142 

spores, action of germicides on, 145 

spores, arthrogenous, 144 

spores, endogenous in, 143 

spores, resistance of, to heat, 144 

staining of, 149, 150 

sterilization b}^ heat, 144 

sterilization, intermittent, 144 

straight, 141 

sj^mbiosis in, 148 

thermophilic, 144 

toxin-forming, 146 

transportation of, with dust, 147 

tube cultures, 153 

vacuoles in, 

variations, artificial, in, 148 

variations in form, 141, 143 

varieties in. 148 

virulence of, as influencing infection, 
163 

zoogloea form of, 142 

zymogenic, 146 
Bacterisemia, nature of, 179 
Bacterial emboli, 161 



776 



INDEX. 



Bacterial examination of post-mortem 
specimens, 37 
flora of body, 159 
products, action of, in body, 160 
toxins, 161 

toxins, action of, in body, 160 
Bactericidal action of tissues, 160 
Bacterio-protein, 161 
Bailey and Eicing on Landry's paral5'sis, 

ref. 757 
Balanitis, 650 
Balantidum coli, 129 

Baldwin on carcinoma of pancreas, ref. 532 
Barker, ref. on Bacillus pj^ocyaneus, 188; 
on nervous system, 730 ; on regeneration 
in nerve tissue, 739 
Barloic's disease, 336 
Basedovfs disease, 332 
Batten on nerve lesions in diphtheria, ref. 

236 
Baurngarten on vessels of heart, ref. 404 
Becker on rhabdomyoma, ref. 656 
Benda on miliary tuberculosis, ref. 218 
Beri-beri, 251 
Bernlieini and Gruher on mixed infection, 

ref. 165 
Berry on appendicitis, ref. 518 
Bert and Lamh on Malta fever, ref. 241 
Bezangon and Lahle on role of the h'mph- 

nodes in infection, ref. 160 
Bichloride of mercury, use of, as a fixative, 

54 
Biedl and Kraus on elimination of bacteria 

in secretions, ref. 160, 577 
Biggs on dissecting aneurism of aorta, ref. 

420 
Bile ducts, dilatation of, 561 
ducts, examination of, 31 
ducts, lesions of (see Liver), 559 
ducts, occlusion of, 561 
ducts, perviousness of, test at autopsy, 

31 
typhoid bacilli in, 212 
Biliary calculi, 562 

calculi, role of micro-organisms in, 563 
Bilirubin in blood, 353 
BircTi-Rirschfeld on intestines as portal of 

entry for bacteria, ref. 523 
Bircli-RirscTifeld and Ga,rtert on trans- 
plantation of embryonal cells, ref. 267 
Bizzozero on classification of tissues in 
reference to phj^siological regeneration, 
ref. 94 
Bladder, gall, lesions of, 559 
Bladder, urinary, absence of, 592 
urinary, calculi of, 598 
urinary, congestion of (see Hyperae- 

mia), 595 
urinary, cysts of, 598 
urinary, dilatation of, 593 
urinary, diverticula of, 593 
urinary, examination post mortem of, 

34,43 
urinary, ex stro version of, 593 
urinary, foreign bodies in, 598 
urinary, haemorrhage of, 595 
urinary, hernia of, 594 



Bladder, urinary, hypera^mia of, 595 

urinar}^ hypertrophy of, 593, 596 

urinary, inflammation of (see Cystitis), 
595 

urinary, inflammation of, tubercu- 
lous, 596 

urinary, malformations of, 592 

urinary, parasites of, 598 

urinary, perforation of, 594 

urinary, rupture of, 594 

urinary, tumors of, 597 

urinary, Avounds of, 594 
Black death, 242 
Black -leg, 245 
Blastomycetes, 140, 156 
Blennorrhcea, 176 
Blocqand Marinesco on Friedreich's ataxia, 

ref. 751 
Blood, air in, 354 

alkalinity of, 342 

bacteria 'in, 181, 354 

bilirubin in, 353 

carbonic oxide, effects of, on, 327 

cells, red, agglutination of, 214 

cells, red, altitude, influence of, on, 
347 

cells, red, changes in, 343 

cells, red, degeneration in, 357 

cells, red, diapedesis of, in inflamma- 
tion, 69, 111 

cells, red, diminution of, 343 

cells, red, formation of, 105 

cells, red, nucleated, 347 

cells, red, number of, 343 

cells, red, origin of, 344 

cells, white, changes of, 347 

cells, white, emigration of, 70 

changes in asphyxia, 44 

changes in position after death, 4 

changes of, 342 

changes of, in malaria, 258 

circulation, changes in, 69 

clots, disappearance of, after haemor- 
rhage, 70 

coagulability of, 342 

crises, 347 

degenerative changes in, 351 

endothelial cells in, 353 

examination, methods of, 352 

extravasation of, 69 

fat in, 353 

flow of, in vessels, in accordance with 
the laws of mechanics, 108 

foreign bodies in, 353 

forming organs, changes in, 342, 355 

gases in, 354 

in general diseases, 355 

malarial parasites in, 252 

method of examination of, in malaria, 
259 

parasites in, 354 

pigment in, 351 

platelets in thrombi, 73 

post-mortem changes in composition 
of, 5 

post-mortem changes in distributioD 
of. 9 



IXDEX. 



777 



Blood, pus cells in, 353 
regeneration of, 105 
shadows, 87 
serum, antitoxic, 171 
serum, as culture medium, 152 
serum, germicidal powers of, 125 
tumor cells in, 353 
typhoid bacilli in, 212 
vessels, 410 

vessels, amyloid degeneration of, 82 
vessels, atroph}^ of, 410 
vessels, development of, in regenera- 
tion and repair, 104 
vessels, In^pertropli}' of, 410 
vessels, new formation of, 104 
vessels of brain, lesions of, 730 
vessels of spinal cord, lesions of, 730 
vessels, regeneration of, 99, 104 
vessels, tuberculosis of, relation to 
miliary tuberculosis, 218 
Blue, methylene, as staining agent, 60 
Blumei\ ref. on glandular mj^omata, 619; 
on tuberculosis of the aorta, 417; on tu- 
berculosis of the stomach, 498 
Bod}^ protective mechanism of, 159 
Boils (see Furuncle), 176 
Bone, abscess of, 663, 668 
aneemia of, 677 
atroph}^ of, 661 

bibliography of lesions of, ref. 
Schmidt, 682 
• caries of, 673 
changes in ansemia, 677 
changes in leukgemia, 677 
congestion of (see Hypersemia), 661 
cysts of, 681 

decalcification of, methods, 55 
dermoid cysts of, 682 
enostoses of, 679 
examination of, in infants, 43 
exostoses of, 679 
formation in muscle, 693 
fracture of, healing of, 662 
haemorrhage of, 661 
hypersemia of, 661 
hyperostoses of, 679 
inflammation of, 663, 665 
inflammation of, syphilitic, 665, 666, 

670 
inflammation of, tuberculous, 665, 666, 

670 
lesions of, following typhoid fever, 

211 
leuksemic, 667 

marrow, changes in ansemia and leu- 
kaemia, 677 
necrosis of, 672, 673 
osteomalacia, 677 
osteophytes of, 679 
rachitis in, 674 
regeneration of, 105 
repair of, 105 
rickets in, 674 
sequestrum in necrosis, 672 
softening of, 677 
suppuration of, 663 
syphilis, congenital, of, 671 



Bone, syphihs of, 665, 666. 670 
tuberculosis of, 665, 666, 670 
tumors of, 678 
ulceration of, 673 
wounds of, healing of. 662 
Borst, ref. on inflammation, 126 ; on sacral 

tumors, 276 
Bostroem, ref. on tumors of pia mater, 708 
Bothriocephalus, 134 
Bottomley, ref. on operation in tuberculous 

peritonitis, 524 
Bouillon as culture medium for micro- 
organism. 152 
Bovaird, ref. on endothelial h^'perplasia of 
spleen, 380; on tuberculous lymph- 
nodes. 368 
Brain, abscess of, 718, 752 
actinomycosis in, 764 
anaemia of, 721 
aneurisms of, 723 
apoplexy of, 722 
atrophy of, 719 

axis, method of separation of, at post- 
mortem examination, 15 
blood-vessels of, 720 
blood-vessels, lesions of, 730 
changes of, in general paresis of the 

insane, 759 
condition of, after drowning, 47 
congestion of (see Hj^pergemia), 721 
cysts in, 767 
degeneration of, after embolism and 

thrombosis, 720 
degeneration of, after injuries, 717 
degeneration, systemic, 740 
embolism of, 727 

examination, post-mortem, of, 10, 42 
fixative and hardening method for, 16 
haemorrhage of, 722 
hernia of, 715 
holes in, 767 
hyperaemia of, 721 
hypertrophy of, 719 
inflammation, chronic, of, 758 
inflammation of (see Encephalitis), 751 
inflammation, syphilitic, 763 
injuries of, 717 
injuries, repair of, 100 
in new-born, appearance of, 42 
lacerations of, 718 
lobes of, 11 

location of lesions of, 11 
malformations of, 714 
mantle, method of separation of, at 

post-mortem examination, 15 
methods of study of, 769 
MeynerVs method of opening of, 11, 14 
oedema of, 722 
parasites of, 767 
pigmentation of, 720 
red softening of, 728 
removal of, at autopsies of the new- 
born, 41 
sand, 697, 699, 707, 714 
sclerosis of, 758 
softening, inflammatory, 752 
softening of, 728 



78 



INDEX. 



Brain, staining, methods for, 769 

syphilis of, 763 

thrombosis of, 727 

tuberculosis of, 705, 762 

tumors of, 764 

ventricles, lesions of, 711 

weight of, 11, 42 

"wet," 722 

white softening of, 728 

yellow softening of, 728 
Branchial clefts, carcinoma of, ref. Poioers, 
490 

cysts, 489 
Breast, lesions of (see Mamma), 641 
Breus on cysts with ciliated cells in ute- 
rine myoma, ref. 619 
Brieger and Elirlich on experimental 

lesions of spinal cord, ref. 737 
Bright 's disease (see Nephritis), 572 
Brigidio and Piccoli, ref. on pseudo-leukae- 
mia, 361; on retention of persistent thy- 
mus to Ilodgkiii's disease, 387 
Brill and Lihman, ref. on calcification of 

liver, 544 
Bronchi, 438 

casts of, 440 

dilatation of, 441 

haemorrhage of, 438 

inflammation of (see Bronchitis), 438 

lymph-nodes of, 442 

obliteration of, 441 

ossification of, 442 

post-mortem examination of, 25 

preservation of, 25 

trabeculation of, 439 

tumors of, 442 
Bronchiectasia, 441 

tuberculous, 471 
Bronchiolitis, exudative, 440 
Bronchitis, capillary, 438, 455 

catarrhal, acute, 438, 439 

catarrhal, chronic, 439 

croupous, 440 

exudative, 438 

pseudo-membranous, 440 
Broncho-pneumonia, 455 

excitants of, 458 

tuberculosis, 468 
Bronze skin, 88 

Brooks, ref. on acromegaly, 337 
Brosch, ref. on oesophageal diverticula, 491 
Broth as culture medium, 152 
Brouardel, ref. death and sudden death, 50 
Broion and TJiiry on diphtheritic septicfe- 

mia, ref. 237 
Bubonic plague, 242 
Bvclibinder on intestine as portal of entry 

for bacteria, ref. 523 
Bnckhardt on renal tumors, ref. 592 
Buday on ciliated epithelium in adenoma 

of the breast, ref. 645 
Burns, death from, 49 
Bu8se on renal tumors, ref. 592 
Butler, ref. on membranous enteritis, 515 
Biittner on peritonitis, 523 

Cachexia in tumors, 265 



Cachexia strumipriva, 331 
Cadaveric lividity, 4, 30 
Caecum, inflammation of, 515 

inflammation of, tuberculous, 515 
Calcareous infiltration, 86 
Calcification, 86 

of arteries, 411 

of cerebral vessels, 730 

of heart, 402 

of kidneys, 570, 586 

of liver, 544 

of muscle, voluntary, 691 

of myoma, 618 

of penis, 651 

of pericardium, 389 

of pleura, 435 

of spleen capsule, 379 

of tonsils, 488 
Calculi, biliary, 562 

pancreatic, 533 

preputial, in penis, 651 

prostatic, 659 

renal, 590 

seminal vesicles, 657 

tonsillar, 488 

urinary forms of, 598 
Callus in healing bone, 663 
Campbell on leptothrix, ref. 202 
Cancer (see Carcinoma), 308 
Canon and Pielicke on the bacillus of 

measles, ref. 251 
Cantharides, poisonous effects of, 325 
Capillaries, lesions of, 425 
Capp on aneurism of coronary arteries, ref. 

420 
Caput succedaneum, 41 
Carbolic acid, avoidance of, as a fixative, 

61 
Carbonic oxide, poisonous effects of, 327 
Carbuncle, 176, 197 
Carcino-adenoma, 307 
Carcinoma, 305, 308 

characters of, 308 

"colloid," 318 

cylindrical-celled, 317 

degeneration in, 312 

encephaloid, 318 

extension of, 310 

fibrous, 317 

flat-celled, 312 

forms of, 312 

gelatinous, 318 

medullary, 318 

melanotic, 319 

metastatic, 310 

molle, 318 

multiple, 312 

myxomatodes, 319 

of adrenals, 386 

of arteries, 421 

of bladder, 597 

of bone, 681 

of brain, 765 

of branchial cleft, ref. Powers, 490 

of bronchi, 442 

of dura mater spinalis, 709 

of Fallopian tubes, 640 



INDEX. 



779 



Carcinoma of gall bladder and ducts, 561 

of heart. 410 

of intestine, 520 

of kiduej^s, 592 

of Uuynx, 432 

of liver, 555 

of lung, 480 

of lympli-nodes, 370 

of mamma, female, 645 

of mamma, male, 660 

of mouth, 848 

of muscle, 693 

of nerves, 767 

of oesophagus, 492 

of ovaries, 632 

of pancreas, 532 

of parotid, 529 

of penis, 651 

of pericardium, 390 

of peritoneum, 525 

of pharynx, 490 

of pleura, 437 

of prostate, 659 

of seminal vesicles, 657 

of spleen, 380 

of stomach, 501 

of testicles, 656 

of thyroid, 384 

of tongue, 485 

of tonsil, 490 

of urethra, male, 601 

of uterus, 622 

of vagina, 606 

of veins, 425 

of vulva, 604 

scirrlius, 317 

simplex, 317 

squamous-celled, 312 

telangiectoides, 318 
Caries of bone, 673 
Carnitied lungs, 446 
Carnoy\s fluid, formula, 51 
Cartilage, regeneration of, 105 
Carvochromes, 731 
Caseation, 91 
Caspar, ref. 39 
Casts, renal, 566 

renal, methods of fixation of, 54 

renal, resembling corpora amvlacea, 
83 
Catarrh, purulent, 176 
Catarrhal inflammation, 128 
Cavities, bronchiectatic, 441 

formation of, in jDulmonary tubercu- 
losis, 474 
Cell, body, function of, 95 

changes, progressive, 78 

changes, retrogressive, 78 

characters, hereditary, maintenance 
of, 261 

dependence and independence of, 66 

division, amitotic, 97 

division, indirect, 95, 97 

division, mitotic, 95 

division, modes of, 95 

energy, phases of, 65, 78 

gro^vth, most active period of, 94 



Cell " inclusions " in tumors, 270 

nucleus, function of, 95 

physiological control in, reproduction 
of, 262 

proliferation, most active periods of, 
94, 261 

regeneration, characters and limita- 
tions of, 98 

regeneration, conditions which incite, 
105 

regeneration, phj^siological, 94 

regeneration, ref. to Fuerst, 278 

reproduction, abnormal, 262 

reproduction, physiological, in adult, 
262 

types, conditions of maintenance of, 
261 

Wilson on the, ref. 272 
Cells, action of bacterial products on, 161 

cancer, 309 

complex organization of, 95 

dead, characters of, 90 

dead, fibrin formation under influence 
of, 112 

embryonal, transplantation, ref. Birch- 
Hirschfeld and Garten, 267 

eosinophile, germicidal powers of, 125 

formation of, in granulation tissue, 118 

formative stimulus in growth of, 272 

ganglion, mitosis in, 99 

ganglion, nature and structure of, 780 

mast-, 288. 848 

necrosis of, 90 

new-formed, recognition of, 98 

plasma-, 103 

"prickle," in epithelioma, 813 

restoration of, after degeneration and 
injury, 99 

spider, in glioma, 297 

spined, in epithelioma, 818 

white blood-, 347 
Celloidin, use of, for embedding, 55 
Centrosome, significance of, 95 
Cephalhiematoma in the new-born, 41 
Cephalocele, 715 
Cercomonas intestinalis, 129 
Cerebellar ataxia, 751 
Cerebrospinal meningitis, 194 
Cerebrum, lesions of (see Brain), 714 
Cerenxille, Tavel, etc., on bacterial exci- 
tants of colitis, ref. 514 
Cestoda, 131 
Chalk stones, 335 
Chancre, 232 

Chancroid, bacteria of, 197 
Charbon, 197 

symptomatique, 245 
C liar cot- Ley den crystals, 351, 678 
Clieese poisoning, 828 
Cheesman and Meltzer, on local lesions and 

tissue vulnerability^ ref. 160 
Cheesy degeneration, 91 

degeneration in tuberculosis, 220 
Cheloid. 280 
Chemistry, importance of, in pathology, 

68 
Chemotaxis by dead cells, 125 



780 



INDEX. 



Cliemotaxis iu bacteria, 145 

nature of, 111 

negative, 125 
" Chest serum " as culture medium, 152 
Cliiari on auto-digestion of pancreas, 529 

on typhoid fever without characteris- 
tic lesions, 212 

ref. on obliterating phlebitis in hepa- 
tic vein, 538 
Children, causes of sudden death in, 50 

changes in, immediately after birth, 
40 

new-born, age, characters, and size of, 
40 

new-born, autopsies of, method of, 39 
CMttenden and Alhro, on skin pigment, 

88 
(Chloral hydrate, poisonous effects of, 327 
Chloroform, poisonous effects of, 327 
Chloroma, 291 
Chlorosis, 355 
Cholangitis, 559 
Cholecystitis, 559 
Cholelithiasis, 562 
Cholera asiatica, 214 

asiatica, bacterial diagnosis of, 216 

asiatica, experimental in animals, 216 

asiatica, lesions of, 215 

spirillum, group of spirilla resemblins:, 
217 
Cholesteatoma, 294 
Cholesterin in fatty degeneration, 80 
Chondroma, 296 

of bone, 679 

of bronchi, 412 

of choroid plexus, 714 

of clitoris, 604 

of dura mater cerebralis, 698 

of dura mater spinalis, 709 

of heart, 410 

of larynx, 432 

of liver, 556 

of lung, 480 

of lymph-nodes, 370 

of mamma, 645 

of mouth, 484 

of muscle, 693 

of ovaries, 632 

of parotid, 528 

of pia mater cerebralis, 707 

of submaxillary gland, 528 

of testicles, 656 

of veins, 425 
Chondro-sarcoma, 291 
Choroid plexus, cj^sts and tumors of, 714 
Chromatic figure in mitosis, 96 
Chromatin, changes of, in cell division, 95 

changes of, in necrosis, 90, 91 
Chromatolysis, 736, 738 

of ganglion cells in sunstroke, 335 
Chromophylic bodies, 731 

bodies, method of staining, 770 
Chromosomes in mitosis, 95 
Chyle vessels, dilatation of, 426 
Chylous ascites, 426, 521 
Cicatricial tissue, damage by, 126 
Cicatrix, nature of, 119 



Circulation of the blood, changes in, 69 
Circulatory system, 387 

system, sudden death from lesions of, 
49 
Cirrhosis of liver, 546 

of liver, congenital, 551 
Cladothrix, 143 
Clitoris, malformations of, 602 

tumors of, 603 
Clostridium forms of bacteria in, 141 
Clots, apoplectic, 722 

heart, 23, 398 
Cloudy swelling (see Albuminous Degen- 
eration), 79 
Coagulation necrosis, 90 
Goats on tumor of pineal gland, ref. 768 
Cobhett and MeUome on granulation tissue 

and infection, ref. 160 
Cocci, 140 

growth, forms of, 142 

packet forms of, 142 

variations in form of, 141 
Coccidia, 129 

in liver, 559 

in Paget' s disease, 641 
Coccidium oviforme, 129 
Coccus, "chain," 185 

golden, 182 
Colinheim on embolism, ref. 76 
Cohnheim's hypothesis of etiology of 

tumors, 269 
Colchicum, poisonous effects of, 325 
Colitis, amoebic, 511 

bacterial, 512 

catarrhal, acute, 510 

chronic, 515 

croupous, 513 

diphtheritic, 513 

excitants of, 514 

fibrinous, 515 

follicular, 512 

infections, acute, 511 

membranous, 515 

mucous, 515 

necrotic, 514 

nodular, 512 

pseudo-membranous, 513 
"Colloid" cancer, 318 

degeneration, 85 

nature of, ref. to ReinbacJi, 383 
Colocynth, poisonous effects of, 325 
Colon bacillus, 187 

bacillus, comparison with Bacillus ty- 
phosus, 214 

dilatation of, 505 

group of bacilli, 189 

malpositions of, 503 

tumors of, 518 

ulcers of, 512, 513, 515 
Combined system disease, 750 
Commensals, bacterial, 148 
Compound granular corpuscles, 729 
Concretions of appendix, 517 

of intestines, 520 

of pancreas, 533 

of prostate, 659 

of seminal vesicles, 657 



INDEX. 



781 



CondoUon on tabes, ref. 749 
Conclvloma of penis, 650 . 

of vulva, 603 

syphilitic, 233 
.Cone on chronic gastritis, ref. 196 
Congenital infection, 165 
Congestion (see Hvpersemia) 

of the blood, 69 

post-mortem, 9 

pulmonary, 443, 444 

relation of hyperplasia to, 121 
Couium, poisonous effects of, 328 
Connective tissue, importance of, in -re- 
pair, 99 

tissif^, new formation of, 102 

tissue, regeneration of, 102 

tissue, repair by, 102 
Constitutio lymphatica, 337 
Contagious diseases, 167 
Contagium, 167 
Contusions, appearances of, after death, 

7 
Cooling of the body, post-mortem, 5 
Coplin on branchial cysts, ref. 486 
Copper poisoning, effects of, 325 
Cornet, ref. on scrofula, 368 

on tuberculosis, 230 
Cornil and Carnot on regeneration of mu- 
cous membranes, ref. 101 
Coronary arteries, lesions of (see Heart) 

arteries, post-mortem examination of, 
24 
Corpora aliena articulorum, 685 

amylacea, 83 

cavernosa, inflammation of, 650 
Corpus luteum, changes in, 631 
Corrosive sublimate, fixative, use of, as, 54 

sublimate, germicidal action of, 145 

sublimate, poisonous effects of, 324 
Cotton swabs for collecting culture mate- 
rial, 155 
Councilman, ref. on interstitial nephritis, 
575 

on lung lobule. 449 

on sudden death due to heart, 394 

on arterio-sclerosis, 416 
Councilman and Lafleur on amoebic dys- 
entery, ref. 129 
Councilman, Mallory, and Pearce on diph- 
theria, ref. 236 
Councilman, Mallory, and Wright on cere- 
brospinal meningitis, ref. 195 
Covyie on differentiation between tuber- 
cle and smegma bacilli, ref. 229 
Cou^pefs glands, lesions of, 659 
Coyon on micro-organisms of stomach, 497 
Crabs, regeneration of lost parts in, 99 
Cramer on nerve lesions in sunstroke, 335 
Craniotabes, 675 

Cranium, examination of base of, at autop- 
sies, 15 

examination of, in infants, 14 

opening of, in adults, 9 
Crenothrix, 143 
Cretinism, sporadic, ref. to Osier, 331 

thj-roid, relation of, to, 331 
Croton oil, effect of, on stomach, 32 



Croton oil, poisonous effects of, 325 
Croupous bronchitis, 440 

inflammation (see Fibrinous Inflam- 
mation), 123 
Croioder on generalized tuberculous 

lymphadenitis, ref. 368 
Cryptorchismus, 652 
Culex, 255 
Cullen, ref. on rapid fixation and frozen 

section m e t h o d, 52 ; on glandular 

myomata of uterus, 619; on hydro- 
salpinx, 638; on uterine tuberculosis, 

614; on carcinoma of uterus, 622 
Cultures, bacteria, 151 ^ 

of bacteria, methods of study, 153 

of post-mortem material, methods of 
securing, 37 
Cunningham, ref. on death from electrical 
currents, 48 

on experimental thj^roidism, 331 
Curschmctnn on typhoid cystitis, ref. 596 
Curschmctnn' s spirals, 440 
Cushing, ref. on bacteria and biliary cal- 
culi, 563 

on gonococcal peritonitis, 523 
Cyanosis in cardiac malformations, 392 
Cyclopia, 714 
Cylindroma, 294 
Cystadenoma of mamma, 645 

of ovaries, 632 

papillary of ovaries, 636 
Cysticercus, 132 

of brain, 767 

of heart, 416 
, of kidney, 592 

of muscle, 694 

of pia mater, 708, 710 

of peritoneum, 526 

of spleen, 380 

of ventricles of brain, 714 
C3"stitis, acute catarrhal, 595 

chronic, 593 

croupous, 596 

diphtheritic, 596 

emphysematous, 596 

exudative, 595 

necrotic, 596 

tuberculous, 596 

typhoid, 596 
Cystocele in female, 604 

vaginal, 594 
Cj^sto-sarcoma, 290 
Cysts, 277 

atheromatous, of arteries, 413 

branchial, 486 

ciliated, ref. to Hess and Zcthn, 278 

closure of, by granulation tissue, 120 

congenital, 278 

dermoid, of lung, 480 

dermoid, of nose, 429 

dermoid, of ovary, 637 

dermoid, of spleen, 380 

dermoid, of thja-oid, 384 

disintegration, 277 

follicular, of ovary, 636 

foreign body, 277 

formed about blood clots, 70 



782 



INDEX. 



Cysts, methods of preparation of, 61 

of bone, 681 

of brain, 724, 767 

of clioroid plexus, 714 

of Cowper's glands, 660 

of ependjnna, 714 

of Fallopian tubes, 640 

of Graafian follicles, 636 

of kidney, 589 

of larynx, 482 

of liver, 555, 556 

of liver with renal cysts, 589 

of mamma, 647, 660 

of mediastinum, 481 

of mesentery, 526 

of mouth, 484 

of oesophagus, 493 

of omentum, 526 

of ovaries, compound, 632, 636 

of pancreas, 532 

of parovarium, 637 

of pia mater cerebralis, 708 

of pericardium, 390 

of placenta, 628 

of pleura, 437 

of prostate, 659 

of salivary glands, 528 

of scrotum, 651 

of seminal vesicles, 657 

of spinal cord, 766 

of stomach, 503 

of testicles, 656 

of tongue, 485 

of trachea, 432 

of tumors, 277 

of urethra, male, 601 

of urinary bladder, 598 

of uterus, 627 

of vagina, 606 

of vulva, 604 

retention, 277 
' retro-ovarian, 640 

retroperitoneal, 526 

sebaceous, of penis, 651 

transudation, 277 
Cytolog3% importance of modern studies 

in, 66 
Cytoplasm, function of, 95 

Dagonet on tumors of dura mater, ref. 698 
Balims on differential stains for tubercle 

and smegma bacilli, ref. 229 
Bavenport, ref. experimental morphology, 

111 
Davis, ref. on diabetic gangrene, 334 
Dead bodies, data for identification of, 4 

putrefactive changes in, 5 

tissues, changes in, 89 

tissues, disposal of, in body, 92 
Death, black, 242 

causes of, determination of, 3 

from asphyxia, 44 

from burning, 49 

from drowning, 46 

from electricity, 48 

from hanging, 45 

from strangulation, 45 



Death from suffocation, 44 

from violence, lesion in, 44 

sudden, causes of, 49 

sudden, from heart, ref. Councilman, 
394 

sudden, from tumor emboli, 266 

sudden, lesions in, 44 

sudden, lesions leading to, 3 

time of, as determined by post-mortem 
appearances, 6 
Decalcification of bone, methods for, 55 
Deciduoma of placenta, 628 

of uterus, 626 
Decomposition, post-mortem, 5 
Defensive proteids, 169 
Degeneration, 79 

acute, 79 

albuminous, 79 

albuminous, restoration of cells after, 
99 

amyloid, 82 

amyloid, of adrenals, 385 

amyloid, of arteries, 411 

amyloid, of intestine, 506 

amyloid, of kidney, 569 

amyloid, of liver, 542 

amyloid, of lymph-nodes, 363 

amyloid, of muscle, 691 

amyloid, of pancreas, 529 

amyloid, of placenta, 627 

am3doid, of spleen, 372 

amyloid, of stomach, 491 

amyloid, of thyroid, 382 

amyloid, of uterus, 610 

ascending, 743 

cheesy, 91, 220 

colloid, 85 

colloid, in thyroid, 382 

combined system, 750 

descending, 742 

fatty, 80, 81 

fatty, from phosphorus poisoning, 
328 

fatty, of adrenals, 885 

fatty, of arteries, 411 

fatty, of endocardium, 401 

fatty, of heart, 400 

fatty, of joints, 682 

fatty, of kidneys, 568 

fatty, of liver, '541 

fatty, of muscle, 690 

fatty, of pancreas, 529 

fatty, of placenta, 627 

fatty, of prostate, 657 

fatty, of stomach, 494 

fatty, of uterus, 610 

fatty, of veins, 423 

glycogen, 84 

glycogen, of kidneys, 569 

glycogen, of liver, 548 

granular, 79 

granular, in red blood cells, 347 

hyaline, 86 

hyaline, of arteries, 411 

hyaline, of heart, 402 

hyaline, of islands of Langerhans in 
pancreas, 530 



INDEX. 



'83 



Degeneration, hyaline, of lymph-nodes, 363 

hyaline, of muscle, 690 

hyaline, of prostate, 657 

hj^aline, of thjToid, 882 

hydropic, 84 

lardaceous, 82 

mucous, 84 

neurone, 785 

neurone, systemic, 740 

parenchymatous, 79 

polychromatophilic, in anaemia, 345 

primary, of neurones, 744 

relation of, to inflammation, 122 

secondary, following cerebral haemor- 
rhage, 724 

secondary, in nervous S3'stem, 741 

waxy, 82 
Dejeriiie, ref. on ataxic paraplegia, 750 
Bejerine and Letulle, ref. on Friedreich's 

ataxia, 751 
Delafield, ref. on colitis, 510 
Delafield's haematoxyliu stain, 59 
Delamare on syphilitic nephritis, ref. 587 
Delirium tremens, alcohol as excitant of, 

326 
Dendrites, 728 

changes in, from separation from their 
cell bodies, 735 
Denecke, spirillum of, 217 
Dermatitis, blasto-mycetic, 156 
Dermoid cysts of bone, 682 

cj'sts of choroid plexus, 714 

cysts of lung, 480 

cysts of mouth, 484 

cysts of nose, 429 

cysts of peritoneum, 529 

cysts of spleen, 380 

cysts of thyroid, 384 

cysts of urinar}^ bladder, 598 

tumors of mediastinum, 481 

tumors of penis, 651 

tumors of scrotum, 651 

tumors of testicle, 657 
Dermoids of thymus, 381 
DeWitte, ref. on membranous endometritis, 

611 ; on mj'ositis ossificans, 693 
Diabetes, bibliography, ref. to Von Noor- 
den, 334 

"bronzed," 384 

haemachromatosis in, 88 

mellitus, 833. 384 

pancreas lesions in, 530 

phloridzin, 335 

relations of, to internal secretions, 334 

sudden death in, 50 
Diapedesis, 69 

in inflammation, 111 
Diaphragm, portions of, 21, 42 
Diastematomyelia, 716 
Diaster in mitosis, 96 
Digestive system, 482 
Digitalis, poisonous effects of, 328 
Dilatation of heart, 896 
Diphtheria, 235 

antitoxin, 238 

association with tuberculosis, ref. 237 

bacillus of, 287 



Diphtheria, bacteriology of, 286 

concurrent infection in, 237 

diagnosis, bacterial, in, 238 

experimental, 238 

heart lesions in, 286 

lesions of, 235, 236 

nerve lesions in, 236 

pseudo-, 186 

pseudo-, membrane of, 285 

septicaemia, 237 

toxin of, 238 

visceral lesions of, 236 
Diplobacilli, 142 
Diplococci, 142 
Diplococcus intracellularis, 195 

pneumoniae, 190 
Diplomyelia, 716 
Disease, causes of, 67 

contagious, 167 

definition of, 166 

etiology of, 67 

general, 331 

infectious nature of, 164 

nature of, 65 
Disinfectants, action of, on bacteria, 145 
Distoma, 181 

in bladder, urinar}', 598 

in blood, 354 

in liver, 558 
Diverticula false, of intestine, 504 

in veins, 425 

of bladder, 598 

of intestine, 503 

of oesophagus, 491 

of pharynx, 486 
Division of cells, 95 
JDmocliowski, ref. on pyogenic powers of 

typhoid bacilli, 213 
DmocliotcsM and Janowski, ref. on hepatic 

cysts, 555 
Bohroicolski, ref. on lymph-nodules of 

larynx, etc., 488 
Dochmius duodenalis, 136 
Dock, ref. on chloroma. 291 ; on sarcoma 

of stomach, 501 ; on trichomonas, 180 
Doicd, ref. on cysts of the mesentery, 526; 
on tuberculosis of cervical lymph-nodes, 
367 
Dropsy, nature of, 71 

of pericardium, 387 
Drowning, condition of viscera after, 47 

death from. 46 

inspection of body after, 46 

internal examination after, 47 

lesions of, 46 
Drysdale's corpuscles, 685 
Ductus arteriosus in stenosis of aorta, 
421 

arteriosus, malformations of, 891 
Biinlmr, ref. on typhoid fever, 212 
Duodenum, post mortem examination of, 
31 

ulcers of, 508 
Dura mater cerebralis, characters of, 695 

mater cerebralis, examination of, at 
IDOst-mortem examination, 10 

mater cerebralis, haemorrhage of, 695 



784 



INDEX. 



Dura mater cerebralis, inflammation of (see 
Pachymeningitis), 690 
mater cerebralis, inflammation of, tu- 
berculous, 698 
mater cerebralis, syphilis of, 698 
mater cerebralis, thrombosis of, 695 
mater cerebralis, tumors of, 698 
mater spinalis, haemorrhage of, 709 
mater spinalis, inflammation of, 709 
mater spinalis, parasites of, 709 
mater spinalis, tuberculosis of, 709 
mater spinalis, tumors of, 709 

Diirck, ref. on experimental pneumonia, 
459 

Dust, bacteria in, 147 

Dyes, classification of, 345 

Dysentery (see Colitis), 510 
amoeba in, 128 
amoebic, 511 
excitants of, 511 
pyocyaneus, 512 
tropical, 511 

Ear, internal, method of examination at 

autopsies, 16 
Eber on animal tuberculosis, ref. 227 
Ecchymoses, 70 

in asphyxia, 44 

in purpura, 337 

of lung, 445 

post-mortem and ante-mortem. 7 
Echinococcus exogcna, 134 , 

in bladder, urinary, 598 

in blood, 354 

in brain, 767 

in dura mater spinalis, 709 

in heart, 410 

in kidney, 592 

in liver, 557 

in muscle, 694 

in peritoneum, 526 

in pleura, 437 

in prostate, 659 

in spleen, 380 

in testicle. 657 

in veins, 425 

in ventricles of brain, 714 

multilocularis, 134 

scolecipariens, 134 
Eden on the placenta, ref. 627 
Edmunds on Basedow's disease, ref. 332 
Egg albumen, use of, to fasten sections to 

slide, 52 
EhrUcli and Lazarus on anaemia, ref. 352 
Ehrlich's method for blood fixation, 352 
Elaterium, poisonous efi'ects of, 325 
Electrical currents, death from, 48 
Electricity, death from, 48 
Elephantiasis, 426 

of scrotum, 651 

of vulva, 603 
^?;^^?^(7 on gonococcal infection, ref. 192,194 
Embedding, celloidin, 55 

paraffin, 56 
Emboli, bacterial, 161 

fat, 354 

infective, 76, 113 



Emboli, infective, cardiac origin of, 408 

intestinal, 506 

parenchyma cell, 75 

tumor, in arteries, 422 
Embolism, aberrant, 77 

coagulation necrosis in, 91 

effects of, 75 

in brain, 727, 729 

in coronary arteries, 403 

in kidney, 565 

in liver, 113 

in lung, 445 

in mesenteric artery, 506 

in muscle, 692 

in portal vein, 537 

in spinal cord, 729 

in spleen, 374 

in terminal arteries, effects of, 76 

in tumors, 264 

retrograde, 77 
Embolus, nature of, 75 
Embrj^o, age of, method of determining, 
40 

human, general characters and size of, 
at difl'erent ages, 39 

maturity, signs of, 40 
Embryology, relationships of, to pathol- 
ogy, ref. Marcliand and Minot, 274 
Embryos, method of preservation of, 61 
Emigration, a physiological process, 123 

in frog's mesentery, 109 

nature and causes of, 111 
Emphysema, interstitial, 448 

interstitial, from gas bacillus, 243 

of lung, 447 

pulmonary, 447 
Empyema, 176, 435 

excitants of, 436 
Encephalitis, acute, 751 

acute disseminated, 753 

chronic, 758 

exudative, 751 

in new-born, 757 ' . 

parenchymatous, 753 

suppurative, 753 
Encephalocele, 715 
Enchondroma (see Chondroma) 
Endarteritis, 412 

obliterans, 413 

syphilitic, 232 
Endocardial vegetations, 408 
Endocarditis, 406 

acute, 406 

bacteria of, 407 

chronic, 408 

infective, 407 

infective, excitants of, 407 

infective, injury as predisposing to, 
407 

gonococcal, ref. Lartigaii, 407 

malignant, 407 

mycotic, 407 

tuberculous, 409 

ulcerative, acute, 407 

ulcerative, chronic, 408 

ulcerative, malignant, 407 

ulcerative, simp2e, 407 



INDEX. 



785 



Endocardium, characters of, 406 

fatty degeneration of, 401 

lesions of, 406 
Endometritis, catarrhal, 611 

chronic, 611 

croupous, 613 

diphtheritic, 613 

exfoliative, 611 

membranous, 611 

puerperal, 615 

syphilitic, 614 

tuberculous, 613 
Endophlebitis, 423 

chronic, 425 
Endothelial cells as phagocytes, 116 

cells, phagocytic powers of, 125 

sarcoma, 291 
Endothelioma, 291 

bibliography of, 295 

embryological data bearing on, 295 

occurrence of, 295 

of adrenals, 386 

of bone, 681 

of brain, 765 

of dura mater cerebralis, 698 

of dura mater spinalis, 709 

of intestine, 520 

of kidney, 590 

of lung, '480 

of lymph-nodes, 370 

of lymph-vessels, 427 

of nerves, 767 

of ovaries, 632 

of parotid, 528 

of pericardium, 390 

of peritoneum, 525 

of pia mater cerebralis, 707 

of pleura, 437 

of spinal cord, 765 

of submaxillary gland, 528 

of thymus, 381 

of thyroid, 384 

of uterus, 619 
Endothelium, changes in, favoring throm- 
bosis, 73 

changes of, in liver, in typhoid fever, 
209 

changes of, in syphilis, 232 

formation of connective tissue from, 
104 

lesions of, in typhoid fever, 207 

or mesothelium, 115 

secretory capacities of, 71 

■' selective filtration " by, 112 

vascular, in inflammation, 109 
Energy cell, 65 
Engelken on renal adenoma in children, 

ref . 591 
Enostoses, 679 
Enteritis, 506 

catarrhal, acute,' 506 

catarrhal, chronic, 507 

croupous, 507 

diphtheritic, 507 

exudative, 507 

follicular, 507 

membranous, 515 

50 



Enteritis, nodular, 507 

pseudo-membranous, 507 

suppurative, 507 

syphilitic, 508 

tuberculous, 507 
Enteroliths, 520 
Enteroptosis, 27 
Enzymes, bacterial, 146 
Eosinophile cells, destruction of germs by, 
. 125 
Ependyma, cysts of, 714 

method of hardening of, 16 

tumors of, 714 
Ependymitis, acute, 711 

chronic, 712 
Epicardial fibroid nodules, 390 
Epididymitis, 653 
Epispadias, 649 
Epithelial metaplasia, 94 

pearls in epithelioma, 313 
Epithelioma, 313 

giant-celled, 317 

gland-like, 316 

neuro-, 317 
Epithelium, amitosis in, 102 

formation of, in healing wounds, 119 

regeneration of, 99, 101 
Epulis, 287 
Ernst on psammoma, 699 

ref. on chondroma, 296 
Erosions, h£emorrhagic, of stomach, 500 
Erysipelas, 185 

Erythrosin, contrast stain in NissVs meth- 
od, 770 
Esser on disturbances of pulmonary cir- 
culation, 445 
Ether, poisonous effects of, 327 
" Eulenburg on Basedow's disease, ref. 332 
EiDing, ref. on blood changes in diseases 

of liver, 554; on ganglion cells, 737; 

on ganglion cells in typhoid fever, 

211; on lymphatic constitution, 338; 

on malarial nephritis, 577; on toxic 

leucocytosis, 350 
Exanthemata as types of contagious dis- 
eases, 167 
Exophthalmic goitre, 332 
Exophthalmus, 332 
Exostoses, 297, 679 
Extra-uterine pregnancy, 640 
Exudates, disposal of, after inflammation, 
112 

formation of, in inflammation, 109 

inflammatory, 113 

inflammatory, removal of, 112 

in suppurative inflammation, 176 

methods of fixation of, 54 

nature of, 72 

significance of, in inflammation, 126 
Exudative inflammation, 108 
Eyes, method of removal of, at autopsies, 
16 

Falkson on tumor of pineal gland, ref. 768 
Fallopian tubes, absence of, 638 

tubes, closure of. 638 

tubes, cysts of, 640 



786 



INDEX. 



Fallopian tubes, dilatation of, 638 
tubes, fluid in hydrosalpinx, 638 
tubes, foetus, development of, in, 640 
tubes, lisemorrliage in, 638 
tubes, inflammation of (see Salpingi- 
tis), 639 
tubes, inflammation, syphilitic, of, 639 
tubes, inflammation, tuberculous, of, 

639 
tubes, length of, 36 
tubes, malformations of, 638 
tubes, malpositions of, 638 
tubes, post-mortem examination of, 36 
tubes, tumors of, 639 
Famine fever, 241 
Farcin de boeuf, 201 
Farcy, 195 

Farner on Basedow's disease, ref. 332 
Fat crystals in degeneration, 80 
emboli, 354 

formation of, from protoplasm, 80 
in blood, method of demonstrating, 

353 
in necrotic tissue, 90 
Infiltration of, in atrophied muscle, 689 
necrosis, 92 

pericardial, atrophy of, 394 
Fatigue, eifect of, on neurones, 739 
Patty degeneration, 80, 81 

infiltration, 80, 81 
Fehleisen, streptococcus of, ref. 185 
Fenomenocles on hydatid nodes of placenta, 

ref. 628 
Fenioick on sarcoma of stomach, ref. 501 
Ferment, fibrin-forming, 112 

substances formed b}^ cells, 92 
substances in phagocytosis, 116 
Fermentation and micro-organisms of, ref. 
to Jorgenson, 156 
relation of, to bacteria, 146 
Ferments, bacterial, 146 
Fetzer on fibrinous bronchitis, ref. 446 
Fever, catarrhal, epidemic, 202 
famine, 241 
hospital, 247 
jail, 247 
Malta, 241 
puerperal, 180 
relapsing, 241 
scarlet. 250 
seven<Iay, 241 
ship, 247 
spirillum, 241 
surgical, 180 
spotted, 247 
traumatic, 180 
typhoid, 203 

typhoid, concurrent infection in, 212 
typhoid, modes of infection, 213 
typhoid, preventive inoculation in, 213 
typhoid, secondary lesions, 210 
typhus. 247 
yellow, 248 
Fibrin, action of, in limiting toxic effects, 
126 
formation of, in inflammation, 112 
in blood clots, 70 



Fibrin in thrombi, 73 
Fibrinogenous substance, 112 
Fibrinous inflammation, 123 
Fibroblasts, 103, 118 
Fibro-carcinoma, 317 
Fibroma, 279 

intracanalicular, 282, 644 

mixed, 280 

moUuscum, 279 

cedematous, 283 

of appendix, 520 

of bladder, urinary, 597 

of bone, 678 

of brain, 764 

of bronchi, 442 

of dura mater cerebralis, 698 

of dura mater spinalis, 709 

of ependyma, 714 

of Fallopian tubes, 639 

of gall bladder and ducts, 561 

of heart, 410 

of intestine, 518 

of joints, 685 

of kidney, 590 

of larynx, 432 

of liver, 555 

of lungs, 480 

of lymph-nodes, 370 

of mamma, 643, 660 

of mouth, 484 

of muscle, 693 

of cpsophagus, 492 

of ovaries, 631 

of parotid, 528 

of penis, 651 

of pericardium, 390 

of peritoneum, 524 

of pharynx, 489 

of pia mater cerebralis, 707 

of pleura, 437 

of scrotum, 651 

of spinal cord, 765 

of spleen, 380 

of stomach, 500 

of submaxillary gland, 528 

of testicles, 656 

of tongue, 485 

of vagina, 606 

of vulva, 603 

pericanalicular, of mamma, 644 

polypoid, 280 
Fibro-m3^oma, 298 
Fibro-myxoma, 282 
Fibro-sarcoma, 285 
Fibrosis, 122 

relation of, to inflammation, ref. 
Aclami, 122 
Fibrous tissue, formation of, in repair, 117 
Filamentous bacteria, 142 
Filaria in bladder, 598 

in kidney, 592 

in lymph-nodes, 370 

medinensis, 137 

sanguinis hominis, 138 

sanguinis hominis in blood, 354 
Findler, on specimen of hair ball of stom 
ach, ref. 503 



INDEX. 



787 



Mnkler on pneumonia, ref. 202 
FinMer and Prior, Vibrio proteus, 217 
Fischer on false diverticula of intestine. 

ref. 504 
Fischl on foetal infection, ref. 166 
Fish poisoning, 328 
Fistulse, branchial, 486 
vesico-vaginal, 605 
Mtz on dilatation of colon, ref. 505 
on lesions of pancreas, 531 
on pancreatic cysts, 533 
Fixation of special forms of cells in fluids, 
membranes, etc., 54 
of tissue elements, 51 
of tissues, importance of, 61 
rapid, of tissues, 51 
Flagella of bacteria, 140 

of malarial parasite, 256 
Flechsig on tabes, ref. 749 
Flemming's osmic acid mixture, formula 

and uses of, 53 
Fletcher on tuberculous cavities in liver, 

ref. 553 
Flexner, ref. on abrin and ricin intoxica- 
tion, 178 
on experimental pancreatitis, 531 
on fatty degeneration of heai't muscle, 

401 
on focal lesion in liver in tj^phoid 

fever, etc., 209 
on focal necrosis, 179 
on glioma of retina, 317 
on lymphosarcoma, 360 
on peritonitis, 523 
on plague pneumonia, 457 
on syphilis of stomach, 498 
on terminal infection, 166 
on toxalbumin intoxication, 162 
on tropical dj^sentery, 512 
on tuberculous oesophagitis, 492 
on typhoid bacilli in endocarditis, 
213 
Flexner and Anderson on B. diphtherite 

in the lungs, ref. 237 
Flexner and Barker on bacteriology of 

cerebrospinal meningitis, ref. 195 
Flockemann on pulmonary syphilis, ref. 

480 
Flukes, 130 
" Foamy " liver, 557 

Focal lesions in viscera in typhoid fever, 
208, 209 
necrosis, 178 

necrosis in diphtheria, 236 
Foetal infection, 165 

tissues, preservation of, 43 
Foetus, age, general characters, and size 
of, at different ages, 39, 40 
maturity of, signs of, 40 
syphilis of nervous sj'stem in, 763 
Food poisoning, 161 
Ford on bacteriologj^ of healthy organs, 

ref. 159 
Formalin, disinfectant action of, 145 

use of, in fixation of tissue, 53 
Formative stimulus in cells, 105 
stimulus in tumor growth, 272 



Foulerton on pathogenic blastomycetes, 

ref. 156 
Fractures, intra-uterine, 41 

post-mortem appearance of, 8 
Fragmentation of heart muscle, 402 
Freeborn, formula of, for picro-acid f uch- 

sin, 60 
Freeman, ref. on fatty liver in infants, 541 

on milk and tj^phoid fever, 213 

on typhoid fever and oysters, 213 

on vaccination, bibl. 250 
Freezing method for sections, 51 

microtome, use of, 52 
Fresh tissues, methods of study, 51 
Frieberger and Frohner on animal pathol- 
ogy, ref. 260 
Friedemann on tonsils as portals of entrv, 

ref. 489 
Friedemann and Maas on extirpation of 

the hypophysis, 337 
Friedlander, pneumo-bacillus of, 189 
Freidreich on ataxia, ref. 751 
Friedreich's ataxia, 751 
Frog, study of inflammation in mesentery 

of, 108 
Frozen sections, methods for, 51 
Fuchsin, use of, in staining tubercle ba- 
cilli, 223 
Fuerst, ref. on cell regeneration, 273 

on giant cells, 116 
Fungi, poisonous effects of, 326 
Fungi, fission-, 140 

mould-, 140 

yeast-, 140 
Fungus, mould-, 156 

ray-, 200 
Furuncle, 176 

Gall bladder, calculi of, 562 

bladder, dilatation of, 561 

bladder, infection of, 561 

bladder, lesions of (see Liver), 559 

bladder perforation in typhoid fever, 
210 

bladder, tumors of, 561 

ducts, calculi of, 562 

ducts, lesions of (see Liver), 559 

ducts, tumors of, 561 
Gamboge, poisonous effects of, 325 
Gametes of malarial parasite, 257 
Ganglia, semilunar, post-mortem examina- 
tion of, 33 
Ganglion cells, changes in body of, from 
lesions to dendrites. 737 

cells, chromatolysis of, 737 

cells, chromatolysis of, in sunstroke, 
335 

cells, mitosis in, 99 

cells, nature and structure of, 730 

cells, Nissl's method of staining, 770 
Gangrene, 90 

after embolism, 76 

diabetic, 334 

emphysematous, 244 

of appendix, 517 

of lung, 448 

of mouth, 483 



788 



INDEX. 



Gangrene of pancreas, 53 

of vagina, 606 

of vulva, 603 
Gaseous phlegmon, 244 
Gastritis, catarrhal, 495 

chronic, 495 

croupous, 496 

diphtheritic, 496 

exudative, 497 

membranous, 496 

phlegmonous, 497 

suppurative, 497 

syphilitic, 498 

toxic, 497 

tuberculous, 498 
Gastro-intestinal canal as portal of entry 
for micro-organism, 160 

canal exterior to body tissues, 159 
Gaylord on origin of fibrin, etc. , ref . 434 
Gelatin as culture medium, 152 
Gemmules of ganglion cells, 732 
General diseases, 331 

pathology, 63, 65 
Genito- urinary organs, post-mortem exam- 
ination of, 34, 43 
Gentian violet in Oram's stain, 150 
Germicidal action of body fluids, 125 

action of cells, 125 

action of tissues, 160 
Germicides, 145 
Germs, 140 
Gerulanos on dermoid tumors of penis, 

ref. 651 
Giamiettasio on umbilical tumors, ref. 526 
Giant cells as phagocytes, 116 

cells, formation of, 116 

cells, formation of, in amitotic cell 
division, 98 

cells in tubercles, 219 
Giant-celled sarcoma, 286 
Gigantoblasts, 347 

OUchrist, ref. on blastomycetic dermatitis, 
156 

on fibroma molluscum, 280 

on parasitic excitants of tumors, 272 
Gill clefts, cysts of, 486 
Gland epithelium, regeneration of, 102 
Glanders, 195 

group of bacilli, 197 
Glioma, 297 

of adrenals, 386 

of brain, 764 

of ependyma, 714 

of spinal cord, 766 
Glio-sarcoma, 286 
Olockner, ref. on endothelioma, 295 

on endothelioma of pleura, 437 
Glossitis, 485 
Glottis, oedema of, 430 
Glucose, use of, in culture media, 152 
Oluge's corpuscles, 718; 729 
Glycerin, avoidance of, as a fixative, 61 
Glycogen infiltration, 84 

stains for, 84 
Glycosuria, 334 
Goitre, 383 - " 

exophthalmic, 332 



Gonococcus, 192, 193, 194 

Gonorrhoea, 192 

Goodale on tonsillitis, ref. 488 

Goppert on pseudo-leuksemia, ref. 361 

Gordirder and Lartigau on typhoid pleu- 

ritis, ref. 436 
Gottstein on micro-organisms in air, ref. 

159 
Gout, 335 

joint lesions in, 684 
Graafian follicles, cysts of, 636 

follicles, haemorrhage of, 629 
Graham on displacements of liver, ref. 

534 
Grauis method of staining bacteria, 150 
Granular degeneration, 79 
Granulation tissue, 118 

tissue in wound infection, ref. to Afa- 
nassieff, Cobbettand Melsom, andJur- 
cjelunas, 160 
Granulations, exuberant, 120 
Granuloma, 278 
Grass bacillus, 229 
Grates' disease, 332 
Grawitz on blood examination, ref. 352 
Gregariuae, 129 
Griffith on aneurism of coronary arteries, 

ref. 420 
Grippe, see influenza, 202 
Grober on pleural infection, ref. 436 
Guinea worm, 137 
Gumma, syphilitic, 232 
Gun-cotton, use of, as celloidin in embed- 
ding, 55 
Guthrie on tuberculosis in children, ref. 

228 
Guy and Ferrier on forensic medicine, ref. 

48, 328 
Gicyn on typhoid bacilli in bile, ref. 212 

Hjemangioma, 303 

Haematin, use of, in haematoxylin stain, 59 

Haematocele, 653 

uterine, 610 
Haematogeuesis, defective, 343, 344 
Haematoidin, 344 

in blood clots, 70 

in pigment, 87 
Haematoma, 70 

of pia mater cerebralis, 706 
Haematometra, 607 
Haematomyelia, 726 
Haematomyelopore, 727 
Haematophilia, 71 

Haematoxylin, DelafiekVs formula and uses 
of, 59 

iron, Heidenhain's, 59 
Haemochromatosis, 88 
Haemoglobin, decomposition of, 87 
Haemoglobinaemia, 343, 344 
Haemoglobinuria, 71, 344 
Haemolysis, 87, 344 

excessive, 343, 344 
Haemorrhage, 69 

conditions favoring, 70 

from oesophageal varices in cirrhosis, 
550 



INDEX. 



789 



Haemorrhage in adrenals. 385 

in bladder, 595 

in bone, 661 

in brain, 722 

in bronchi. 438 

in dura mater cerebralis, 695 

in dura mater spinalis, 709 

in Fallopian tubes, 638 

in foetal head during labor, marks of, 
41 

in heart valves, 397 

in intestine, 506 

in liver, 535 

in lung, 445 

in mamma, 64 

in muscle, 692 

in new-born, 71 

in oesophagus, 490 

in ovaries, 629 

in pachj^meningitis, 697 

in pancreas, 531 

in penis, 650 

in pericardium, 387 

in pia mater cerebralis, 700 

in pia mater spinalis, 710 

in pineal gland, 768 

in placenta, 627 

in pleura, 433 

in spinal cord, 725 

in stomach, 494 

in thymus, 381 

in uterus, 607, 609 

in vulva, 602 

intermeningeal, 700 

intestinal, in typhoid fever, 210 

removal of clot after, 70 
Hsemorrhagic diathesis, 70, 71 

infarction, 70, 76 

inflammation, 123 

infection, ref. to Honh 337 

septicaemia, 243 
Haemorrhoids, 423 

urethral, 601 
Hsemosiderin, 87, 344 
Raff Mile's method of preventive inocula- 
tion in Asiatic cholera, 216 

method of preventive inoculation in 
bubonic plague, 242 

method of preventive inoculation in 
typhoid fever, 213 
Hair balls in stomach, 503 
Hall on lesions of bronchial lymph-nodes, 
. ref. 443 
Halliburton's Text-book of Chemical Phj^s- 

iology and Pathology, ref. 161 
Hamburger on lymph formation, ref. 71 
Hanging, lesions of, 45 

post-mortem marks of, 7 
Hanseman on tumors, ref. 273 
Hardening and preservation of tissues, 51 

of tissues, agents for, 52 
Hare, medical complications of tvphoid 
fever, ref. 213 

on tumors of the mediastinum, 481 
Haiiser on fibrin formation, ref. 112 
Hay bacillus, 229 
Hayem's solution for blood fixation, 352 



Head, post-mortem examination of, 9 
Healing by first intention, 108 

by second intention, 120 

influence of cell types in, 99 

of wounds, 116 

process in wounds, variations in, 119 
Heart, abnormal size of, 393 

abscess, embolic, of, 403 

absence of, 392 

aneurism of, 397 

aneurism of coronary arteries of, 420 

atrophy of, 394 

atrophy, brown, of, 394 

calcification of, 402 

chordae tendineae, abnoi-mal, in, 392 

clots, 23, 398 

condition of, after drowning, 47 

coronary arteries, examination of, 24 

coronary arteries, thi'ombosis of, 402 

degeneration, albuminous, of, 400 

degeneration, amyloid, of, 402 

degeneration, fatty, of, 400 

degeneration, hyaline, of, 402 

degeneration, parenchymatous, of, 400 

dilatation of, 396 

displacements of, 390, 393 

duplicate, 392 

emboli, tumor tissue in, 400 

embolism, infection of, 403 

endocardium, inflammatory lesions of 
(see Endocarditis), 409 

examination, post-mortem, of, 22, 42 

fibrous hyperplasia of, 405 

fragmentation of muscle of, 402 

hypertrophy of, 395 

hypoplasia of, 337, 338, 393 

in infants, lesions of, 42 

in infants, weight of, 42 

infarction of, 404 

Inflammation of, 403 

inflammation, endocardial (see Endo- 
carditis), 406 

inflammation of (see Myocarditis), 403 

interior of, post-mortem examination 
of, 24 

malformations of, 390 

malpositions of, 390, 392 

method of removal of, from body, 22, 
23 • 

necrosis, embolic, of, 404 

parasites of, 410 

pericardial lesions (see Pericardium), 
387 

polypi, 398 

position of, 21, 22 

position of valves and openings of, 
22 

post-mortem staining of, 24 

preservation of tissue of, 24 

reptihan, 391 

segmentation of muscle of, 402 

septa, abnormal, 392 

size of valvular openings of, 23 

syphilis of, 406 

thrombi, with tumor metastases, 400 

thrombosis of, 398 

thrombus, organized, of, 399 



'90 



INDEX. 



Heart thrombus, tuberculous, 399 

transposition of, 398 

tuberculosis of, 406 

tumors of, 410 

tumors of, pericardial, 390 

valves, method of determining com- 
petency of, 22 

valves of, fenestration of, 392 

valves of, malformations of, 392 

valvular openings of, method of meas- 
uring, 23 

vegetations on endocardium, 406 

ventricles, thickness of walls of, 24 

uncovered area of, 22 

weight of, 24 

weight of, in hypertrophy, 395 

wounds of, 393 
Heart-valves, fenestration of, 396 
Heart-valves, hgemorrhage in, 397 
Heat exhaustion, 335 
Heidenlmiii' s iron hgematoxylin, 59 
Heinz on origin of fibrin, etc., ref. 434 
Hektoen on cardiac abnormalities, ref. 392 

on giant cells, ref. 116 

on pathogenic blastomycetes, 158 

on segmentation and fragmentation of 
the myocardium, 402 
Hektoen and Herrick on sarcoma of liver, 

ref. 556 
Helhing on rhabdomyoma, ref. 300 
Held' 8 contrast stain in JSissVs method, 

ref. 770 
Hellebore, poisonous effects of, 325 
Hepatic vessels, lesions of, 537 
Hepatitis (see Cirrhosis), 544 

acute, 544 

chronic, 546 

exudative, 544 

interstitial, 546 

purulent, 544 

syphilitic, 551 

tuberculous, 552 
Hepatization of lungs, 450 
Heppner on hermaphroditism, ref. 649 
Herdman and Boyce on typhoid fever and 

oysters, ref. 213 
Heredity, importance of, in cell life, 66 

significance of mitosis in, 97 
Hermaphrodites, 649 
Hermaphroditism, 649 
Hernia, intestino-vaginal, 604 

of brain, 715 

of lung, 443 

of ovary, 629 

of urinary bladder, 594 

of uterus, 609 

vesico-vaginal, 604 
Herpes of penis, 650 
Hess on ciliated cysts, ref. 278 
Heterotopia, cell, as predisposing factor in 
tumors, 269 

false, of spinal cord, 717 

in spinal cord, 716 
Hintze and Lubarsch on elimination of 

bacteria in secretions, ref. 160 
Hirscli on streptococcus enteritidis, ref. 
514 



Hiss on t3"phoid and colon bacilli, ref. 214 
Hiss and Atkinson on antitoxic substances, 

ref. 171 
Hodenpyl, ref. on absence of spleen, 371 

on actinomycosis in lungs, 200 

on anthracosis, 462 

on appendicitis, 518 

on primary tuberculosis of pleura, 436 

on tonsils, ref. 488 
HodenpyVs modification of Cullen'sTaQt'hod. 

for frozen sections, 52 
Hodgkin's disease, 360 

disease, lesion of lymph-nodes in, 370 
Hoen on lesions oi^the uvula, ref. 487, 691 
Hofmeier on the human placenta, I'ef. 628 
Honl on hsemorrhagic infections, ref. 337 
Housell on malignant tumors of tonsils, 

ref. 490 
Hospital fever, 247 
Howard, ref. on bacteriology of nose, 429 

on extra-intestinal lesion induced by 
the typhoid bacillus, 210 

on htemorrhagic septictiemia, 245 

on pneumobacillus of Friedlander, 189 

statistics of cardiac hypertrophy, 396 
Hoicard and Hoover on tropical abscess of 

liver, ref. 545 
HowsMp's lacunae, 666 
Hueter on congenital tumors of intestine, 

ref. 518 
Huguenin on the excitant of smallpox, 

ref. 249 
Hurdon on endothelioma of uterus, ref. 

619 
Hyaline degeneration, 86 

thrombi, 75 
Hydatid moles of placenta, 628 
Hydatids, 132 

Hydra, regeneration after injury in, 99 
Hydrgemia, 843 
Hydrencephalocele, 715 
Hydrocele, 652 
Hydrocephalus, 711 

acute, 705 

chronic, 712 

congenital, 713, 715 

externus, 715 

internal chronic, examination and re- 
moval of brain in infants, 41 

primary, in adults, 714 

secondary, 713 
Hydromeningocele, 715 
Hydrometra, 607 
Hydromyelia, 716 
Hydronephrosis, 588 
Hydropericardium, 887 
Hydrophobia, 245 

artificial immunity in, 172 
Hydropic degeneration, 84 

infiltration of muscle wall, 691 
Hydropneumothorax, 433 
Hydrops cystidis felleos, 561 
Hydrorrhachis, 716 
Hydrosalpinx, 688 
Hydrostatic test of respiration in infants, 

42 
Hydrothorax, 483 



INDEX. 



791 



Hymen, malformations of, 602 
Hypersemia, 69 

chronic, relation of fibrous hyperplasia 
to, 121 

of bladder, urinary, o95 

of bones, 661 

of brain, 721 

of intestine, 506 

of kidney, 565 

of liver, 585 

of lungs, 443 

of ovaries, 629 

of pia mater cerebralis, 700 

of spleen, 374 

of uterus, 609 

of vulva, 602 
Hyperostosis, 679 
Hyperplasia, 93 

endothelial, of spleen, 379 

fibrous, of heart, 405 

fibrous tissue, 121 

in relation to fibroma, 282 

of adrenals, 386 

of bronchial mucous membrane, 442 

of lymph-nodes, 364 

of lymphoid tissue in liver, 554 

of lymphoid tissue in typhoid fever, 
206 

of pharynx, 488 

of spleen, 375, 379 

of spleen in leukaemia and pseudo-leu- 
ksemia, 380 

of thymus, 381 

of thyroid, 383 

of tongue, 485 

replacement, 122 

replacement, fibrous, in muscle, 693 

replacement, neuroglia, in nervous 
sj'Stem, 740 
Hyperplastic tuberculous inflammation of 

intestine, 515 
Hypertrophy, 93 

compensatory, 93, 99 

compensatory, ref. to Aschoff, 106 

of bladder, urinary, 593 

of blood-vessels, 410 

of brain, 719 

of heart, 395 

of kidney, 564 

of muscle, 689 

of pineal gland, 768 

of prostate, 657 

of thymus, 381 

of tongue, 485 
Hyphfe of moulds, 156 
Hyphomycetes, 140, 156 
Hypoleucocytosis, 350 
Hypophysis cerebri, lesions of, 768 

extirpation of, ref. to, 337 

relation of, to acromegaly, 337 
Hypospadias, 649 

Ice-cream poisoning, 328 
Ichorcemia, 180 
Ichthyosis of mouth, 483 
Icterus, pigment in, 88 
Immunity, 164 



Immunity, acquired, 169 

anti-microbic, 169 

antitoxic methods of securing, 171 

artificial, 169 

artificial, complex nature of, 173 

artificial, in diphtheria, 172, 288 

artificial, in smallpox, 172 

artificial, methods of securing, 169 

cellular, 169 

definition of, 168 

hereditarj^ 168 

hypotheses concerning, 173 

modes of acquirement of, 169 

natural, 166 

nature of, 168 

toxic, 169 
Immunization, artificial and natural, 169 

artificial, hypotheses concerning, 173 

complex nature of, 178 

specific, 172 
Incarceration of intestine, 504 
Indigo, sulphate of, poisonous action of, 

821 
Infantile spinal paralysis, 755 
Infants, autopsies of, methods of, 89, 41 

change in, immediately after birth, 40 

new-born, general characters and size 
of, 40 
Infarction, coagulation necrosis in, 91 

embolic, 75, 76 

haemorrhagic, 70, 76 

hcemorrhagic pulmonary, 445 

intestinal, 506 

of heart, 404 

of kidney, 565 

of liver, 538 

of lung, 445 

of muscle, 692 

of placenta, 627 

of spleen, 374 

white, 76 
Infection, 164 

concurrent, 165 

concurrent, in pulmonary tuberculo- 
sis, 476 

concurrent, in tuberculosis, 228 

congenital, 165 

cooling of body as predisposing to, 
ref. Reinehoth and Kohlhardt and 
Kisskalt, 460 

forms of, 165 

general liealth, relation of, to, 163 

granulation tissue in, ref. Afanassieff, 
160 

haemorrhagic, ref. to Honl on, 337 

latent, Adami, ref. 160 

leucocytosis in, 349 

mixed, 165 

mixed, in tuberculosis, 228 

nature of, 164 

predisposition to, 168 

proofs of relation of bacteria to, 162 

puerperal, 180 

spleen, role of, in, ref. 376 

sub-, Adami, ref. 160 

terminal, 166 
Infectious diseases, 164, 175 



■■ 



792 



INDEX. 



Infectious diseases, bibliography, 260 

diseases, classification of, 167, 174 

diseases, communicability of, 166 

diseases, conditions influencing occur- 
rence of, 163 

diseases, definition of, 168 

diseases, general considerations con- 
cerning, 174 

diseases of animals, 260 

diseases, predisposition to, 163 

diseases, specific nature of, 174 

diseases, suppurative, 175 
Infective granulomata, 278 
Infiltration, calcareous, 86 

fatty, 80, 81 

fatty, of heart, 402 

fatty, of liver, 540 

glycogen, 84 

serous, 84 
Inflammation, 107 

catarrhal, 123 

characterization of, 126 

cicatricial tissue following, 119 

conditions determining phases of, 122 

conservative in character, 124 

croupous, coagulation necrosis in, 91 

definition of, 127 

exudative, 108, 118, 120, 122 

exudative, in mesentery of frog, 109 

fibrinous, 123, 177 

following injury from micro-organ- 
isms, 113 

formation of granulation tissue in, 118 

general considerations, 107 

haemorrhagic, 123 

in non-vascular tissue, 108 
. infectious, 113, 123 

interstitial, 121 

meaning of, 124 

muco-purulent, 123 

mucous, 123 
■ necrotic, 123 

of adrenals, 385 

of appendix, 517 

of arteries, 412 

of bladder, urinary, 595 

of bone, 663, 665 

of brain, 751 

of caecum, 515 

of Cowper's glands, 659 

of dura mater cerebralis, 696 

of dura mater spinalis, 709 

of Fallopian tubes, 639 

of heart, 403 

of intestine, 506 

of intestine, large, 510 

of joints, 682 

of kidney, 570 

of liver, 544 

of lung (see Pneumonitis), 449 

of lymph -nodes, 364 

of mamma, 641 

of mediastinum, 481 

of muscle, 692 

of nerves, 757 

of oesophagus, 492 

of ovaries, 629 



Inflammation of pancreas, 531 

of parotid, 526 

of penis, 650 

of pericardium (see Pericarditis), 388 

of periosteum, 663 

of peritoneum, 521 

of pharynx, 487 

of pia mater cerebralis, 701 

of pia mater spinalis, 710 

of placenta, 627 

of pleura, 433 

of portal vein, 536 

of prostate, 658 

of spinal cord, 753 

of spleen, 375 

of stomach, 495 

of testicle, 653 

of thymus, 381 

of thyroid, 383 

of tongue, 485 

of tonsils, 488 

of urethra, 600 

of uterus, 611 

of vagina, 605 

of vascular tissue, 108 

of veins, 423 

of ventricles of brain, 711 

of vulva, 602 

original conception of, 107 

phases of relationship of, 123 

productive, 117, 122, 123 

pseudo-membranous, 186 

purulent, 123 

regenerative, 122 

relation of hyperplasia to, 121 

relation of injury and degeneration 
to, 107 

relationship of, to normal processes, 
123 

repair after, by first intention, 108 

reparative, 117, 122, 123 

reparative, conservative character of, 
126 

reparative, relation of, to normal proc- 
esses, 124 

resolution in, 115 

sero-fibrinous, 177 

sero-purulent, 123 

serous, 123, 177 

significance of, 123 

special phases of, 122 

suppurative, 123, 175, 176 

suppurative, bacterial excitants of, 
176, 181, 187 

tuberculous, 217 

tuberculous, diffuse, 221 

tuberculous, focal, 218 

types of,' 108 
Inflammatory exudates, action, conserva- 
tive, of, 26 

exudates, disposal of, 112 

exudates, significance of, 124 

fever, 180 
Influenza, 202 

bacillus group, 203 
Infusoria, 129 
Inhibition, sudden death from, 50 



INDEX. 



793 



Insane, paresis, general, of, 759 
Insects, 139 

as conveyors of micro-organisms, 160 

poisonous bites of, 327 
Insolation, 335 
Internal secretions, 329 

secretions, alterations of, in Addison's 
disease, 333 

secretions, nature of, in thyroid, 331 
Intestinal mycosis, 198 
Intestine as portal of entrv for bacteria, 
ref. 523 

as portal of entry for micro-organisms, 
160 

bacteria of, ref. 514 

bibliography of lesions of, ref. Thorel, 
520 

cloacae of, 504 

concretions of, 520 

congestion of, 506 

degeneration, amyloid, in, 506 

discoloration, post-mortem, of. 30 

diverticula of, 503 

embolism and thrombosis of vessels 
of, 506 

examination, post-mortem, of, 30, 43 

haemorrhage of, 506 

hyperaemia of, 506 

incarceration of, 504 

infarctions of, 506 

inflammation of, 506, 510 

inflammation, tuberculous, of, 507, 515 

intussusception of, 505 

large, inflammation of (see Colitis), 510 

large, lesions of, 510 

large, ulcers of, 512, 513, 515 

lesions of, in Asiatic cholera, 215 

lesions of, in infants, 43 

lesions of, in typhoid fever, 204 

malformations of, 503 

opening of, at autopsies, 30 

parasites of, 520 

pigmentation of, after typhoid fever, 
205 

position of. 20 

post-mortem changes in. 20, 30 

preservation of, 31 

removal of, at autopsy, 30 

rupture of, 505 

small, anthrax of, 508 

small, inflammation of (see Enteritis), 
506 

small, inflammation, syphilitic, of, 508 

small, inflammation, tuberculous, of, 
507 

small, ulcers of. 508 

strangulation of, 504 

stricture of, 506 

transposition of, 503 

tuberculosis, hyperplastic, of, 515 

tumors of, 518 

ulceration of, in t3'phoid fever, 206 

wounds of, 505 
Intoxication, bacterial, 161 

nature of, 164 
Intranuclear network, changes of, in cell 
division, 95 



Intussusception of intestine, 505 
Involution forms of bacteria, 141 
Iodine test for am3'loid degeneration, 28, 
83 
use of, in removal of sublimate from 
tissues, 54 
Iron, detection of, in pigment, 87 

haematoxvlin, Heidenliairi's, 59 
Itch insect, 139 

Jacohson on hair balls in stomach, ref. 503 

Jacobstlml on scurvy, ref. 336 

Jail fever, 247 

JakoimM on micro-organisms in thrombi, 

ref. 73 
Jalap, poisonous effects of, 325 
Janowski on suppurative inflammation, 

ref. 178 
Jaundice, pigment in, 88 
Jenner's stain for blood, 353 
Joints, degenerations in, 682 
false, 663 

inflammation of (see Arthritis), 682 
inflammation, tulDerculous, of, 684 
loose bodies in, 685 
suppuration of, 682 
tuberculous, 684 
tumors of, 685 
Jordan on osteomyelitis, ref. 670 
Jores on elastic tissue in arterio-sclerosis, 

ref. 413 «^ 
Jorgenson on micro-organisms and fermen- 
tation, ref. 156 
Josserand and Bonnet on mj^ocarditis with 

ulcerative endocarditis, ref. 403 
Jilrgelunas on granulation tissue and in- 
fection, ref. 160 

Kdlhle on bacteria in lymph-nodes, ref. 

362 
Karj^okinesis, 95, 97 
Karyolysis, 90 
Karj^omitosis, 97 
Karyorrhexis, 90 
Kedroicsky on emphysematous cystitis, 

ref. 596 
Keen on surgical complications of typhoid 

fever, ref. 213 
Kelly, ref. on renal tumors. 592 

on tumors of appendix, 520 
Kelynack on appendix vermiformis, ref. 
518 

on renal growths, 592 
Kidney, abscess of, 571 

absence of, 564 

albuminuria, 566 

anaemia of, 565 

atrophied, 582 

calcification, 570, 586 

calculi in, 590 

casts in, 566 

congestion of (see Hvperaemia), 565 

cysts of, 589 

degeneration, acute, of (see Degenera- 
tion, Albuminous), 567 

degeneration, albuminous, in, 567 

degeneration, amyloid, 569 



794 



INDEX. 



Kidney, degeneration, fatty, 568 
degeneimion, glycogen, 569 
degeneration, parencliymatoiis (see 

Degeneration, Albuminous), 567 
displacement of, 564 
elimination of bacteria by, 577 
embolism in, 565, 571 
enteroptosis of, 27 

examination, post-mortem, of, 37, 42 
glomeruli, development of, ref. Horn- 
ing, 572 
granular, 582 

hardening and preservation of, 28 
horseshoe, 564 
hydronephrosis, 588 
hyperaemia of, 565 
hypertrophy of, 564 
in infants, lesions of, 43 
infarction of, 565 

inflammation of (see Nephritis), 570 
inflammation, syphilitic, of, 587 
inflammation, tuberculous, of, 586 
large red, 582 
large white, 581 
malformations of, 564 
movable, 564 
parasites of, 592 
pelvis, lesions of, 587 
perinephritic inflammation, 588 
Plasmodium malarise in, 577 
post-mortem appearance of, 27 
regeneration of epithelium of, ref. to 

Tliorel, 565 
thrombosis of, 565 
tuberculosis of, 586 
tumors of, 590 

tumors, bibliography of, ref. 592 
ureter, lesions of, 587 
wandering, 564 
weight of, in infants, 27, 42 
Kinnicutt on phlegmonous gastritis, ref. 

497 
Kisskalt on cooling as predisposing to in- 
fection, ref. 460 
Kitasato and Yersiii on the bacillus of 

bubonic plague, 242 
Klebs on malformations of generative or- 
gans, ref. 649 
Klippel and Lefas on lesions of pancreas, 

ref. 532 
KUpstein on experimental pneumonia, ref. 

459 
Knox on supra-arterial epicardial fibroid 

nodules, ref. 390 
Koch, discovery of bacillus of tuberculosis, 

ref. 229 
Koch's method of bacterial culture in solid 

media, ref. 151 
Koplik on the excitant of whooping- 
cough, ref. 251 
Koplik and Van Arsdale on osteomyelitis 

in childhood, ref. 670 
Kotlar on tuberculous heart thrombus, 399 
Krompecher on epithelioma, ref. 316 
Kruse, ref. on groups of bacilli, 190 

on groups of bacterial disease exci- 
tants, 175 



Kruse on protozoa, 128 
Kruse and Pasquale, ref. on bacterial exci- 
tants of colitis, 514 
on infective embolism in liver, 546 
Kilhnau on bacteria in blood, ref. 354 

Labia, haemorrhage in, 602 

oedema of, 602 

tumors of, 603 

veins, varicose, in, 602 
Lachner- Sandoval on streptothrix, ref. 201 
Landry's paralysis, 756 
Lang and Ullmann's resume of syphilis, 

ref. 233 
Lang's solution of mercuric chloride for 

fixation, formula and uses of, 54 
Langerhans, islands of, lesions of, in dia- 
betes, 530 
Langman on snake venom, ref. 327 
Lardaceous degeneration, 82 
Lartigau, ref. on bacteriology of angina, 
488 

on concurrent infection in pulmonary 
tuberculosis, bibliography, 477 

on gonococcal endocarditis, 407 

on M. tetragenus, 189 

on pyocyaneous dysentery, 512 

on typhoid bacilli in foetus, 212 

on typhoid fever without character- 
istic lesions, 212 

on uterine involvement in typhoid 
fever, 211 

on variations in virulence of tubercle 
bacilli, 368 

summary of tuberculosis, 230 
Larvae of reptiles and insects, reproduction 

of lost parts in, 99 
Laryngitis, 430 

catarrhal, acute, 430 

catarrhal, chronic, 431 

croupous, 431 

phlegmonous, 431 

suppurative, 431 

syphilitic, 432 

tuberculous, 431 
Larynx, examination of, in infants, 42 

foreign bodies in (see Suffocation), 44 

inflammation of, 430 

malformations of, 430 

post-mortem examination and preser- 
vation of, 26 

tumors of, 432 
Lead, poisonous effects of, 325 
Learning, suggestion of staining for pho- 
tography, 59 
Le Count on lymphoma, ref. 370 
T^ee, Micromotist's Vade Mecum, ref. 51 
Leiomyoma, 298 

Leith on phlegmonous gastritis, ref. 497 
Lenibke on intestinal bacteria, ref. 514 
Leopold and Levi on aspergillus, ref. 156 
Lepra, 230 

ansesthetica, 764 

bacillus, 231 

bacillus, to differentiate, from B. 
tuberculosis, 225 
Leprosy, 230 



INDEX. 



795 



Leprosy, nerve lesions in, 764 
Leptomeningitis (see Meningitis), 701 
Leptothrix, 142, 143, 201, 485, 609 
Lesser, Atlas of Poison Lesions, ref. 328 
Leucin in necrotic tissue, 90 
Leucocytes as phagocytes, 116 

clianges of, 347 

degeneration, fatty, of, 351 

destruction of bacteria by, 125 

emigration of, 70 

emigration of, in inflammation, 109 

eosinopliile, 348 

formation of, 105 

forms of, in suppuration, 177 

in forming abscess, 114 

in granulation tissue, 119 

in leukaemia, 359 

in suppuration, 176 

mononuclear, 348 

number of, in blood, 348 

phagocytic forms of, 125 

polynuclear neutrophile, 348 

transitional, 348 
Leucocythsemia, 358 
Leucocytolysis, 351 
Leucocytosis, 348 

cachectic, 350 

hypo-, 349, 350 

in infectious diseases, 349 

mixed, 350 

pathological, 349 

physiological, 349 

polynuclear, 349 

polynuclear eosinopliile, 350 

relation of, to infection, 349 

toxic, 349, 350 
Leucomains, 146 
Leucoplakia buccalis, 483 
Leukaemia, 358 

bone changes in, 677 

liver lesions in, 554 

lymphatic, 358, 359 

lymph-nodes, lesions in, 369 

myelogenous, chronic, 359 

pseudo-, 360 

splenic, lesions of, 380 
Lemon pneumococcus meningitis, ref. 195 
Xe^c^?^ on. poisons, ref. 328 
Lihman on sarcoma of intestine, ref. 519 
Lightning, death from, 48 
Lip, hare-, 482 
Lipsemia, 353 
Lipoma, 295 

in muscle, 693 

of appendix, 520 

of brain, 764 

of bronchi, 442 

of dura mater cerebralis, 698 

of dura mater spinalis, 709 

of ependyma, 714 

of Fallopian tubes, 639 

of heart, 410 

of intestine, 518 

of joints, 685 

of kidnev, 590 

of larynx, 432 

of liver, 555 



Lipoma of mouth, 484 

of oesophagus, 492 

of penis, 651 

of peritoneum, 524 

of pia mater cerebralis, 707 

of scrotum, 651 

of spinal cord, 765 

of stomach, 500 

of testicles, 656 

of tongue, 485 

of vulva, 604 
Lissauer on tabes, ref. 748 
Litmus, use of, in culture media, 152 
Litten on embolism, ref. 76 
Liver, abscess of, 544 

abscess, amoebic, 545 

abscess, embolic, 114 

abscess, excitants of, 545 

abscess, large, of, 544 

abscess, metastatic, 545 

abscess, tropical, 544 

abscesses, multiple, 545, 560 

accessory, 534 

anaemia of, 535 

atrophy, acute yellow, of, 539 

bile ducts, constriction of, 561 

bile ducts, dilatation of, 561 

bile ducts, occlusion of, 561 

bile ducts, lesions of, 559 

biliary passages, lesions of, 559 

calcification of, 544 

calculi, 562 

cavities, tuberculous, in, 553 

cholangitis, 559 
- , cholecystitis, 559 

cirrhosis (see Hepatitis), 544, 546 

cirrhosis anthracotica, ref. Welch, 551 

cirrhosis atrophic, 546 

cirrhosis, experimental of, ref. ron 
Heukelom, 551 

cirrhosis, hsemaqhromatosis in, 88 

cirrhosis, haemorrhage from oesopha- 
geal varices in, 550 

cirrhosis, hypertrophic, 550 

cirrhosis, relation of subinfection to, 
ref. Adami, 551 

congestion of (see Hyperaemia), 535 

cysts of, 555, 556 

cysts of, with renal cysts, 589 

degeneration, albuminous, of, 539 

degeneration, amyloid, of, 542 

degeneration, fatty, of, 541 

degeneration, glycogen, of, 543 

degeneration, parenchymatous, 539 

destruction of micro-organisms in, 160 

discoloration, post-mortem, of, 33 

displacements of, 534 

effect of tight lacing on, 32 

emboli, infection of, 545 

embolic abscess in, 113 

embolic infarctions in, 77 

enteroptosis of, 27 

examination, post-mortem, of, 32. 43 

"foamy," 243, 557 

furrows in, 32 

gall bladder, dilatation of, 561 

gall bladder, inflammation of, 559 



796 



INDEX. 



Liver, gall ducts, inflammation of, 559 

gall ducts, lesions of, 559 

gas cysts in, 243 

germicidal action of, ref. Adami, 551 

grooves in, 32 

gummata of, 552 

ha-morrliage of, 535 

hardening specimens of, 33 

"hob -nail, "547 

holes in, 557 

hyperaemia of, 535 

infarctions in, 77, 538 

infiltration, fatty, of, 540 

inflammation of (see Hepatitis), 544 

inflammation of, syphilitic, 551 

inflammation of, tuberculous, 552 

lymphoid tissue of, hyperplasia of, 554 

malformations of, 534 

necrosis, from bacteria, 113 

"nutmeg," 536 

parasites of, 557 

perihepatitis, 553 

pigment in, 88, 543 

position of, 20 

regeneration of, 102 

removal from body at autopsy, 32 

rupture of, 535 

size of, 32 

syphilis of, 551 

tuberculosis of, 552 

tumors of, 554 

vein, hepatic, lesions of, 538 

vessels of, lesions of, 537 

weight of, 32, 43 

wounds of, 535 
Limngood on sarcoma of oesophagus, ref. 

492 
Lobelia inflata, poisonous effects of, 328 
Lochte and Sultan on h y p e r p 1 a s i a of 

thymus, ref. 381 
Lockjaw, 239 
Locomotor ataxia, 745 

ataxia, excitants of, 749 
Lofflefs bacillus of diphtheria, 235 

methylene blue solution, 151 
Loomis on cardiac syphilis, ref. 406 
Louse, 139 

Low on appendicitis, ref. 518 
Lowit on hypoleucocytosis, ref. 350 
Liiharscli, ref. on classification of tumors, 
276 

on adrenals, 333 

on branching forms of B. tuberculosis, 
222 

on endothelioma, 295 

on foetal infection, 166 

on parenchyma cell emboli, ref. 75 

on tumors, ref. 273 

on tumors, summary of, ref. 319 
Lungs, 438 

abscess of, 457 

absence of, 443 

accessory, 443 

anaemia of, 443 

anthracosis of, 462 

as portals of entry for micro-organ- 
isms, 449 



Lungs, asphyxia, lesions in, 44 

atelectasis of, 446 

bacteria in, ref. Beco, 459 

broncho- pneumonia of, 455 

broncho-pneumonia, tuberculous, 468 

brown induration of, 444 

carnified, 446 

circulator}^ disturbances in, 443 

circulatory disturbances in, ref. Esser, 
445 

condition of, after drowning, 47 

congestion, chronic, of, 444 

congestion, hypostatic, of, 444, 458 

congestion of (see Hyperaemia), 443 

diphtheria bacilli in, 237 

embolism in, 445 

emphysema of, 447 

examination, post-mortem, of, 25, 42 

gangrene of, 448 

haemorrhage, 445 

hepatization of, 450 

hernia of, 443 

hydrostatic test of respiration, 42 

hyperaemia of lungs, 443 

induration, brown, of, 444 

infarction of, 445 

inflammation of (see Pneumonitis), 449 

inflammation of, tuberculous. 462 

inflammation, syphilitic, of, 479 

injection of blood-vessels of, 26 

injuries of, 443 

lesions of, in infants, 42 

lobules of, ref. Councilman, 449 

lymphatics of, ref. Miller, 449 

malformations of, 443 

oedema of, 445 

perforations of, 443 

phthisis, 471 

pigmentation of, 88, 461 

pneumonokoniosis, 462 

portals of infection in, ref. Grohcr, 
460 

post-mortem changes in, 25 

preservation of, 25 

protective mechanism of, 449 

removal of, at autopsy, 25 

respiration, marks of, in infants, 42 

sclerosis of, 462 

streptothrix in broncho - pneumonia, 
201 

structural peculiarities of, 449 

syphilis of, 479 

thrombosis in, 445 

transposition of, 443 

tuberculosis, focal, of, 464 

tuberculosis, miliar}^ acute, of, 464 

tuberculosis, miliary, chronic, of, 467 

tuberculosis, miliary, healed, of, 467 

tuberculous cavities, formation of, in, 
474 

tumors of, 480 
Lupus, 229 

Lustgarten, bacillus of, 232 
Lymphadenitis, 364 (see Lymph -nodes) 

tuberculous, generalized, 368 
Lymphadenoma of mediastinum, 481 
Lymphangioma, 304, 426. 556 



INDEX. 



797 



Lymphangitis, 426 

infective, 426 

syphilitic, 427 

tuberculous, 427 
Lymphatic constitution, 337 

constitution and sudden death, 50 

tissue, 362 
Lymph- follicles, 362 (see Lymph- nodules) 
Lymph formation, ref, to Hamburger on, 

71 
Lymph- glands, 362 (see Lymph-nodes) 
Lymph-nodes, 362 

as bacterial filters, 160 

anthracosis of, 363 

atrophy of, 362 

bacteria in, ref. Kcilble, 362 

bronchial, lesions of, 442 

bronchial, tuberculosis of, 228 

cervical, tuberculosis of, ref. Doii^d, 
367 

character, general, of, 362 

degeneration, amyloid, 363 

degeneration, hyaline, 363 

generalized tuberculous involvement 
of, 368 

germicidal action of, ref. to Manfred i, 

^ 160 

Hodgkin's disease, lesions of, in, 370 

hyperplasia of, 369 

hyperplasia, acute, of, 364 

hyperplasia, chronic, of, 365 

in leukaemia, 369 

in lymphatic constitution, 338 

in pseudo-leukaemia, 370 

inflammation of, 364 

inflammation, chronic, of, 365 

inflammation, interstitial of, 367 

inflammation, suppurative, of, 365 

inflammation, sj^philitic, of, 368 

inflammation, tuberculous, of, 366 

mesenteric lesions of, in typhoid fever, 
208 

parasites in, 370 

pigmentation of, 89, 363 

scrofula, 367 

significance of, 362 

tracheal, lesions of, 442 

tuberculosis of, 366 

tumors of, 370 
Lymph-nodules, 362 

of larynx, etc., ref. DohroiDolski, 485 
Lymphocj^tes, 347 

role of, in granulation tissue, 119 
Lymphocytosis, 350 

Lymphoid tissue, lesions of, in typhoid 
fever. 204 

tissue of pharynx, hyperplasia of, 488 
Lymphoma, 278, 369 

of intestine, 519 

of lung, 480 

of mediastinum, 481 

of stomach, 501 
Lympho-sarcoma, 286 

of mediastinum, 481 
Lymph-vessels, carcinoma of, 311 

characters of, 426 

dilatation of, 426 



Lymph- vessels dissemination of tumor 

cells through, 427 
inflammation of, 426 
tuberculous inflammation, spread of, 

along, 509 
tumors of, 427 

JlacCaUum, ref. on haematozoan infection 
in birds, 257 

on segmentation and fragmentation of 
the myocardium, 402 
McFarlaml on membranous vaginitis, ref. 

605 
Mc Weeney on rupture of the oesophagus, 

ref. 490 
Mace, Traite de Bacteriologie, ref. 188 
Machard on gall-bladder lesions, ref. 559 
Macroglossia, 304, 426, 485 
Madura foot, 201 
Maladie pyocyanique, 188 
Malaria, 252 

aestivo-autumnal type, 253 

bibliography of, 259 

blood in, method of examination of, 
259 

chronic lesions of, 259 

excitant of, 252 

haemosporidia of, 252 

methods of examination of parasite of, 
259 

pigmentation of viscera in, 258, 543 

protozoon of, 252 

quartan type, 252 

spleen, lesions of, in, 377 

tertian type, 252 

visceral lesions of, 258 
Malarial crescents in blood, 253 
Malign ancj^ of tumors, 265 
Malignant oedema, 244 

pustule, 197 
Malformations of adrenals, 385 

of bladder, 592 

of brain, 714 

of clitoris, 602 

of Fallopian tubes, 638 

of heart, 390 

of hymen, 602 

of kidneys, 564 

of larynx, 430 

of liver, 534 

of lungs, 443 

of oesophagus, 490 

of pancreas, 529 

of peritoneum, 521 

of pharynx, 486 

of mamma, 641 

of mouth, 482 

of nymphae, 602 

of oesophagus, 490 

of ovaries, 628 

of penis, 649 

of spinal cord. 715 

of spleen, 371 

of stomach, 493, 503 

of testicles, 651 

of thyroid, 382 

of tongue, 484 



798 



INDEX. 



Malformations of trachea, 430 
of urethra, 599 
of uterus, 606 
of vagina, 604 
of vulva, 602 
Malta fever, 241 
Mamma, abscess of, 641 
absence of, 641 
accessory, 641 
cysts of, 647 
hsemorrhage of, 641 
inflammation of (see Mastitis), 641 
male, lesions of, 660 
malformations of, 641 
nipple, inflammation of, 641 
supernumerary, 641 
syphilis of, 643 
tuberculosis of, 642 
tumors of, 643 
Mallory on lesions of typhoid fever, ref. 

208 
Mallory and Wriglit on pathological tech- 
nique, ref. 51 
Mandelbaum on teratomata of the medias- 
tinum, ref. 481 
Manfredi on germicidal action of lymph- 
nodes, ref. 160 
Mannaberg on protozoa, ref. 128 
Marchand on endothelioma, ref. 295 

on hydatid moles of placenta, ref. 628 
on pathology and embryology, ref. 
274 
MarcM on descending degeneration, ref. 

743 
Marchi's method of hardening and staining 

nerve tissue, 16, 769 
MarcMafava and Bignami on malaria, ref. 

259 
Marcus on intestines as portal of entry for 

bacteria, ref. 523 
Marfan, ref. on concurrent infection in 
pulmonary tuberculosis, 477 
on lymph-nodes of trachea and bron- 
chi, 443 
Marie, ref. on ataxic paraplegia, 750 

on spinal cord, 745 
Marinesco on ganglion cells, ref. 739 
Marrow, bone-, changes of, in ansemia, 677 
bone-, changes of, in leuksemia, 359, 

677 
bone-, hyperplasia of, in anaemia, 344 
Martin and Rennie on cardiac thrombosis, 

399 
Martius, on auto-intoxication, ref. 320 
MascJika on poisons, ref. 328 
Mast cells, 283, 348 
Mastitis, chronic. 642 
exudative, 641 
exudative, excitants of, 642 
suppurative, 641 
syphilitic, 643 
tuberculous, 642 
MaWiews on artificial parthenogenesis, 

ref. 106 
Maxinioio on experimental amyloid degen- 
eration, ref. 83 
Measles, 251 



Meckel's diverticula, 504 
Mediastinitis, 481 
Mediastinum, cysts of. 481 

dermoid tumors of, 481 

inflammation of, 481 

tumors of, 481 
Medico-legal autopsies, 37 
Megaloblasts, 345, 347 
Megalocytes, 345 
Melanyemia, 351 
Melano-carcinoma, 319 
Melano-sarcoma, 286 
Melanuria in melano-sarcoma, ref. 286 
Meltzer, ref. on physiological struggles 
against bacteria, 160 

on pyloric stenosis, ref. 493 
Membranous dysmenorrhoea, 116 
Menetrier on bibliography of transplanta- 
tion of tumors, ref. 267 

on epithelial metaplasia, ref. 94 
Meninges, cerebral, inflammation of (see 

Meningitis), 701 
Meningitis, acute, 701 

cellular, 701 

cerebro-spinal, 194 

cerebro-spinal, bacterial excitants of, 
195 

chronic, 704 

exudative, 701 

relation to infective processes in ear 
and nose, 704 

spinal, 710 

suppurative, 702 

syphilitic, 705 

tuberculous, 705 

typhoid, 211 
Mercuric chloride, use of, in fixation, 54 
Mercury, poisoning by, 321, 324 
Merismopedia, 142 

Merozites of malarial parasite, 253, 257 
Mesentery, cysts of, 526 

embolic lesions of, 506 

thrombosis of vessels of, 506 
Meslay and Parent on tuberculosis of par- 
otid, ref. 528 
Mesothelium, 115, 295 
Messmates, bacterial, 148 
Metachromatic granules in bacteria, 141 
Metaplasia, 93, 94 
Metastases in tumors, 264 

myeloid, 360 
Methyl violet as stain for amyloid, 83 
Methylene blue as staining agent, 60 

blue, Ldffler\s solution, 151 

blue, use of, in staining malarial blood, 
260 
Metritis, acute, 614 

chronic, 615 

puerperal, 615 
Metschnikoff, studies of, on inflammation, 

ref. 124 
MeynerVs method of opening brain, 14 
Microbes (see Micro-organisms), 140 
Microcephalia, 715 
Micrococci, 140 
Micrococcus gonorrhoea, 192 

lanceolatus, 190 



IXDEX. 



799 



Micrococcus lanceolatus, method of stain- 
ing, 192 

meliteusis, 241 

pneiimonite, 191 

pyogenes, 183 

pyogenes aureus, 181 

tetragenus, 189 
Microcytes, 345 

Microgametes of malarial parasite, 256 
Micromillimetre, sign for, 141 
Micron as unit of measure, 141 
Micro-organisms (see Bacteria), 140 

artificial cultivation of, 151 

conveyance of, by insects, 160 

destruction of, in body, 160 

elimination of, from bod}', 160 

entrance of, througli gastro-intestinal 
canal, 160 

in etiology of tumors, 270 

modes of entrance to body, 160 

pathogenic, 164 

protective mechanism of the body 
against, 159 

relations of, to disease, 159 
Microsporon furfur, 157 
Microtome, freezing, use of, 52 

Minot-Blake, value of, for thin sec- 
tions, 56 

Schanze's, 58 

TliomcCs, 58 
Mignot on bacteria and biliary calculi, 

ref. 563 
Miliary tuberculosis, general, 218 
Milk as culture medium, 152 
Miller, ref. on bacteria of uterus, 611 

on lymphatics of lungs, 449 

on renal lipoma, ref. 590 
Minot, ref. on embryological basis of path- 
ology, 274 

on endothelium, 115 

on retrogressive cell processes, 78 
Minot-Blake microtome, 56, 58 
Missick on teratoma of liver, ref. 557 
Mitchell on foreign bodies in appendix, 

ref. 518 
Mitosis, 95 

abnormal phases of, 97 

achromatic figure in, 96 

asymmetrical, 97 

chromatic figure in, 96 

chromosomes in, 95 

diaster phase of, 96 
. division of the cell body in, 96 

in connective tissue, 102 

in epithelium, 101 

in muscle, 101 

monaster phase of, 96 

multipolar, 97 

polar bodies in, 95 

significance of, 97 

variations in, 97 

without cell division, 98 
Moeller on hay bacillus, 229 
Moles, fibrous, of placenta, 628 
Molluscum contagiosum, 129, 319 
Monaster in mitosis. 96 
Moniez on parasites, ref. 139 



Monomorphism in bacteria, 143 

Monte and Berggriin on anaemia in child- 
hood, ref. 361 

Moore on vaccination, bibliograph}*, ref. 
250 

Morf on sarcoma of thyroid, ref. 384 

Morphine, poisonous effects of, 326 

31orrow on leprosy, ref. 231 

MoscTicoiritz on tetanus, ref. 240 

Moser on cardiac tuberculosis, ref. 406 

Mo8ny on tj'phoid fever and oj'sters, 213 

Mosquito in malaria, 255 

Mother marks, 303 

Moulds, 140, 147, 156, 157, 158 

Mouth, bacteria of, 485 
cvsts of, 484 
diphtheria of, 483 

inflammation of (see Stomatitis), 482 
inflammation, syphilitic, of, 484 
inflammation, tuberculous, of, 483 
malformations of, 482 
micro-organisms of, 485 
tumors of, 484 

Mucous degeneration, 84 
inflammation, 123 
membranes, regeneration of, ref. to 

Cornil and Carnot, 101 
patches of mouth, 484 
polyps, 281, 283 

MuJilmann on senility, ref. 78 

Midler, ref. onabrin and ricin intoxication, 
178 
on normal and pathological histology 
of thyroid, 383 

Milllefs fluid, formula and uses of, 53 

Multiple neuritis, 757 

Mummification, 90 

Mumps, 526 

Muscle tissue, regeneration of, 100 
voluntary, abscess of, 692 
voluntar}^ atrophy of, 687 
voluntar3\ bone formation in, 693 
voluntary, calcification of, 691 
voluntary, degenerations of, 690 
voluntary', embolism in, 692 
voluntary, haemorrhage of, 692 
voluntary, hyperplasia, fibrous, of, 

693 
voluntary, hypertrophy of, 689 
voluntary, hypertrophy, pseudo-, of, 

689 
voluntar}^ infarction of, 692 
voluntarj', infiltration, h^Tlropic, 691 
voluntary, infiltration, serous, 691 
vohmtarv, inflammation of (see Myo- 
sitis), 692 
voluntary, injuries of, 691 
voluntar}', parasites of, 694 
voluntary, rupture of, 691 
voluntar}^ tumors of, 693 
voluntary, vacuoles in, 691 
voluntary, necrosis of, 687 

Muscles, pigment in, 88 

Museum specimens, preparation of, 61 

Mussel poisoning. 328 

Mycelium of mould, 156 

Mycosis intestinalis, 198, 508 



800 



INDEX. 



Mycosis pharyngis, 486 
Mycotic endocarditis, 407 
Myelitis, acute, 753 

central, 754 

chronic, 758, 760 

chronic disseminated, 760 

chronic transverse, 760 

parenchymatous, 753 

peripheral, 754 

transverse, 754 

unilateral, 754 
Myelocytes, 350 
Myeloma of bone, 681 
Myocarditis, 403 

acute, 403 

chronic, 404 

gonorrhoeal, ref. Councilman, 403 

infective, 403 

infective, excitants of, 404 

interstitial, acute, 403 

interstitial, chronic, 404 

suppurative, 403 

syphilitic, 406 

tuberculous, 406 
Myocardium, fragmentation of, 402 

segmentation of, 402 
Myoma, 298 

Isevicellulare, 298 

of appendix, 520 

of Fallopian tubes, 639 

of heart, 410 

of intestine, 518 

of kidney, 590 

of oesophagus, 492 

of ovaries, 632 

of stomach, 501 

of testicles, 656 

of uterus, 617 

of vagina, 606 

of veins, 425 

of vulva, 60 1 

striocellulare, 299 
Myomalacia, 404 
Myosarcoma, 291 

of veins, 425 
Myositis, chronic, 692 

exudative, 692 

interstitial, 692 

ossificans, 693 

suppurative, 692 
Myxoedema, 331 
Myxoma, 282 

of bone, 679 

of brain, 764 

of dura mater spinalis, 709 

of heart, 410 

of larynx, 432 

of liver, 556 

of lymph-nodes, 370 

of mamma, 644 

of mamma, male, 660 

of muscle, voluntar3^ 693 

of parotid, 528 

of submaxillary gland, 528 
Myxo-sarcoma of nerves, 767 

Nabothian follicles, 35 



JSaegeli on statistics of tuberculosis, ref. 

227 
Kaevi, congenital, of skin resembling epi- 
thelioma, 316 

vascular, 303 
Neck in strangulation, marks of cord, etc., 

on, 45 
Necrosis, 89 

coagulation, 90, 220 

coagulation, in diphtheria, 235 

fat, 92, 530 

focal, 90, 178, 236 

from action of tubercle bacilli, 220 

from bacteria in liver, 113 

of bone, 672 

of heart, 403, 404 

of muscle, 687 

relation of, to inflammation, 122 

tuberculous, 220 
Necrotic inflammation, 123 

tissues, disposal of, 92 
Neisser and Schdffer on the gonococcus, 

ref. 194 
Nematoda, 134 
Nephritis, arterio-sclerosis in, 585 

atrophic, 582 

classification of, 570 

diffuse acute, 572 

diffuse acute, excitants of, 576 

diffuse acute, exudative type, 575 

diff'use acute, glomerular type, 575 

diffuse acute, interstitial type, 575 

diffuse acute, lesions of glomeruli, 
572 

diffuse acute, lesions of interstitial tis- 
sue, 574 

diffuse acute, lesions of tubules, 573 

diffuse acute, parenchymatous type, 
575 

diffuse acute, persistent, 577 

diffuse acute, productive type, 575 

diffuse acute, variations in type, 575 

diffuse chronic, excitants of, 585 

diffuse chronic, following acute, 577 

diffuse chronic, general considera- 
tions, 578 

ditt'use chronic, indurative type, 582 

diffuse chronic, interstitial type, 582 

diffuse chronic, parenchymatous tvpe, 
580 

diffuse chronic, variations in t5^pe of, 
583 

diffuse, degenerative tj^pe, 575 

diffuse, hsemorrhagic type, 575 

general considerations of, 570 

glomerulo-, 573, 575 

indurative, 582 

interstitial, 582 

malarial, 577 

obliterating endarteritis in, 585 

parenchymatous, 580 

pyelo-, 587 

suppurative, 571 

suppurative, excitants of, 571 

syphilitic, 587 

tuberculous, 586 
Nephroma, hyper-, 276 



IXDEX. 



801 



Nerve tissue, Marclii's method of liarden- 
ing of, 16 

tissue, methods of study, 769 

tissue, regeneration of, 99 

tissue, replacement hyperplasia in, 
740 
Nerves, action of poisons on, 757 

degeneration of. 735 

degeneration of (see Multiple Neuri- 
tis), 757 

degeneration of systems of, 740 

inflammation, chronic, of, 761 

inflammation of (see Neuritis), 757 

injuries to, 718 

leprous inliammalion of, 764 

methods of hardening of, 19 

method of stud}' of, 769 

peripheral degeneratif)n of, in tabes, 
749 

regeneration of, 100, 740 

sympathetic, changes of, in Addison's 
disease, 332 

tumors of, 767 
Nervous system, 695 

system, artefacts of, 17 

system, inflammation, tuberculous, of, 
762 

system, methods of microscopic study, 
"769 

system, neurone theory of, 730 
JSIetter, ref. on excitants of empyema, 436 

on excitants of pleuritis, 435 

on plague, 243 
Neuritis, 757 

chronic interstitial, 761 

multiple, 757 
Neuroglia, nature and structure of, 733 

regeneration of, 100 

relationships of, 274 
Neuroglioma ganglionare of brain, 764 
Neuroma, 300 

amyelinic, 300 

false, 300, 301 

false, of nerves, 767 

fibrillar, 300 

ganglionic, 300 

multiple, 300 

myelinic, 300 

of adrenals, 386 

of liver, 555 

of nerves, 767 

plexiform, 300 
Neurone, changes in, from action of tox- 
ins, 737 

changes in, from injur}' to one of its 
parts, 735 

changes in, from interference with its 
nutrition, 737 

chromatolysis in, 736, 738 

degeneration, 735 

degeneration, primary, of, 744 

degeneration, secondary, of, 741 

degeneration, systemic, 740 

effect of fatigue on, 739 

nature and structure of, 730 

systems, 740 
Heurones, cortico-spinal motor, 741 

51 



Neurones, motor, cortico-spinal degenera- 
tion of, 744 
motor, peripheral and cortico-spinal 

degeneration of, 745 
motor, peripheral degeneration of, 744 
peripheral motor, 740 
sensory, afferent, 741 
sensory, peripheral degeneration of, 
745 
New-born, autopsies of, the internal ex- 
amination, 41 
general characters of, 40 
hiemorrhage in, 71 
Newman on 'malignant tumors of tonsils, 

ref. 490 
Neicton on rupture of the heart, ref. 393 
Nichols, ref. on ganglion cells in tj^phoid 
fever, 211 
on transplantation of tumors, 267 
JSikiforoff's method for blood fixation, 352 
Nipple, inflammation of, 641 
Nissl bodies, 731 

3"'m-rs method of staining nerve tissue, 770 
Nitro-benzole, poisonous effects of, 326 
JVocard and Leclainche on infectious dis- 
eases of animals, ref. 260 
Noelet on staining of malarial blood, ref. 

260 
Noma of mouth, 483 

of vulva, 603 
Normoblasts, 344 
Norris and Larkin on streptothrix, ref. 201 

on streptothrix pneumonia, ref. 458 
Nortlirup on tuberculous bronchial Ij-mph- 

nodes, ref. 368 
Kortliriqj and Crandall on scurvy, ref. 336 
Norton on persistent thymus and sudden 

death, ref. 381 
Nose, 429 

inflammation of, 429 
syphilis of, 429 
tuberculosis of, 429 
tumors of, 429 
Noyes on accessory adrenals in liver, ref. 

385 
Nuck, canal of, cysts of, 604 
Nucleinic acid, relation of, to germicidal 

substances, 125 
Nucleolus, disappearance of, in cell divi- 
sion, 95 
Nucleus of the cell, function of, 95 
Nutmeg liver, 536 

Nutrient media for bacteria, 151, 152 
Nuttall, ref. on insects in conveyance of 
micro-organisms, 160 
on number of tubercle bacilli in spu- 
tum, 227 
Nux vomica, poisonous effects of, 327 
Nymphae, malformation of, 602 

Obermeier, spirillum of, 241 

Odontoma, 297 

CEdema, hydraemic, of brai)\, 722 

malignant, 244 

nature of, 71 

of brain, 722 

of glottis, 430 



802 



INDEX. 



(Edema of labia, 602 

of lung, 445 

of pla mater cerebralis, 700 

punilent, 177 
Oertel on echinococcus multilocularis, ref. 

558 
OerteVs lesion, 188 
(Esopliagitis, catarrhal, 492 

croupous, 492 

pseudo-membranous, 492 

tuberculous, 492 
(Esophagus, action of poisons on, 492 

bibliography of, ref. Thorel, 492 

cysts of, 493 

dilatation of, 490 

diverticula of, 491 

examination, post-mortem, of, 26 

hgemorrhage of, 490 

inflammation of (see (Esophagitis), 492 

inflammation, tuberculous, 492 

malformations of, 490 

perforation of, 490 

rupture of, 490 

stenosis of, 491 

tumors of, 492 

varices of, in cirrhosis. 550 
Oidium albicans, 158, 488, 606 
Oligocythsemia, 343 
Omentum, cysts of, 526 

position of, 20 
Oophoritis, acute, 629 

chronic, 629 

syphilitic, 631 

tuberculous, 631 
Ophuls, ref. on corpora amylacea, 83 

on typhoid fever without characteris- 
tic lesions, 212 
Opie, ref. on fat necrosis, 530 

on haemachromatosis, 88 

on lesions of the pancreas with chole- 
lithiasis, 531 

on ]mncreas in diabetes, 530 

on pancreatitis, 532 
Opitz on intestinal canal as portal of entry 

for bacteria, ref. 523 
Opium, poisono .s effects of, 326 
Oppenheim on multiple sclerosis, ref. 759 
Orchitis, chronic, 654 

exudative, 653 

leprous, 656 

syphilitic, 655 

tuberculous, 654 
Origanum, oil of, for clearing, 56 
Oriental plague, 242 
Orthman on retro-ovarian cysts, 640 
OrtJi's fluid, formula and uses of, 58 
Osier on sporadic cretinism, ref. 381 
Osier and McCrae on carcinoma of stomach 

in the j^oung, ref. 502 
Osmic acid, use of, as fixative and staining 

agent, 53 
Ossification of bronchi, 442 

of muscle, 693 

of penis, 651 

period of, at various centres in foetus, 
39 
Ossification-centre in lower epiphysis of 



femur as sign of maturity or age of the 
foetus, 40 
Osteitis, 665 

condensing, 666, 668 

rarefying, 666 

suppurative, 668 

syphilitic, 665, 666, 670 

tuberculous, 665, 666, 670 

ulcerative, 673 
Osteoclasts, 666 
Osteoid cancer, 681 

chondroma of bone, 679 

tissue, 662 
Osteoma, 296 

malignant, 681 

of bone, 670 

of brain, 764 

of dura mater cerebralis, 698 

of lungs, 480 

of pia mater cerebralis, 707 

of spinal cord, 765 

of testicles, 656 
Osteomalacia, 677 
Osteomyelitis, chronic, 670 

infective, 669 
Osteophytes, 297, 679 
Osteo-porosis, 666 
Osteo-sarcoma, 288 
Osteo-sclerosis, 666, 668 
Ottolengid on pneumonia, ref. 192 
Ovarian pregnancy, 640 
Ovaries, changes in form and size of, 628 

congestion of (see Hyperaemia), 629 

cysts, dermoid, of, 637 

cysts of, compound, 632 

dermoid cysts of, 687 

displacements of, 628 

examination, post-mortem, of, 36 

foetus, development of, in, 640 

haemorrhage in, 629 

herniae of, 629 

hyperaemia of, 629 

inflammation of (see Ovaritis), 629 

malformations of, 628 

situation, size, and shape of, 36 

syphilis of, 631 

teratoma of, 687 

tuberculosis of, 681 

tumors of, 681 

weight of, 36 
Ovaritis, 629 

syphilitic, 631 

tuberculous, 631 
Ovula Nabothi, 35, 612, 627 
Oxyuris vermicularis, 185, 598, 606 
Oysters and typhoid fever, 218 

Pacchionian bodies, 699 

bodies, situation of, 10 
Pachymeningitis, chronic, 697 

externa, 696 

interna haemorrhagica, 697 

interna, 696 

spinalis, 709 

syphilitic, 698 

tuberculous, 698 
Packard on the tonsils, ref. 488 



INDEX. 



803 



Paget's disease, 641 

Palate, cleft, 482 

Pancreas, abnormal forms of, 33 

accessory, 529 

atrophy of, 529 

auto-digestion of, 529 

calculi of, 533 

concretions of, 533 

cysts of, 532 

degeneration, albuminous, of, 529 

degeneration, fatty, of, 529 

discoloration, post-mortem, of, 33 

displacements of, 529 

ducts of, dilatation of, 532 

examination, post-mortem, of, 33 

fat necrosis of, 530 

foreign bodies in, 533 

gangrene of, 531 

haemorrhage of, 531 

hardening and preservation of, 33 

infiltration, fatty, of, 529 

inflammation of (see Pancreatitis), 531 

lesions of, in typohid fever, 210 

malformations of, 529 

necrosis, fatty, of, 530 

parasites in, 533 

pigment in, 88 

relations of, to diabetes, 334 

shape and situation of, 33 

size of, 33 

tumors of, 532 

weight of, 33 
Pancreatitis, bibliography of, ref. 532 

experimental, ref. Flexner, 531 

exudative, 531 

ligemorrhagic, 531 

suppurative, 531 
Papilloma, 280 

of bladder, urinary, 597 

of Fallopian tubes, 640 

of kidney, 590 

of larynx, 432 

of mouth, 484 

of CESophagus, 492 

of ovaries, 631 

of penis, 650 

of peritoneum, 524 

of stomach, 500 

of vagina, 606 

of vulva, 603 
Paraffin, use of, for embedding, 56 
Paralysis, ascending, acute, 756 

Landry's, 756 

spinal, infantile, 755 
Parametritis, 615 
Paraphimosis, 650 
Paraplegia, ataxic, 750 
Parasites, animal, 128 

animal, eggs of, ref. 'd. Jakscli and 
Simon, 139 

bibliography of, 139 

in bladder, urinary, 598 

in blood, 354 

in brain, 767 

in dura mater spinalis, 709 

in heart, 410 

in intestines, 520 



Parasites in kidney, 592 

in liver, 557 

in Ij^mph-nodes, 370 

in muscle, 694 

in pancreas, 533 

in peritoneum, 526 

in pia mater cerebralis, 708, 710 

in prostate, 659 

in spleen, 380 

in testicles, 657 

in th3'roid, 385 

in vagina, 606 

in ventricles of brain, 714 

malarial. 252 

plant, 140 
Parasitic bacteria, 147 
Parenchj'matous degeneration, 79 

encephalitis and myelitis, 753 
Paresis of the insane, general, 759 
Paris green, poisonous effects of, 324 
Park, W. H., Bacteriology in Medicine and 

Surgery, ref. 152 
Park, B. , ref. on deformities from osteomy- 
elitis, 670 

on influenza bacillus, ref. 203 

on tumors, ref. 272 
Parotid, inflammation of, 210, 526 

tuberculosis of, 528 

tumors of, 528 
Parotitis, 526 
' Parovarium, cysts of, 637 
Parsons on bone lesions in typhoid fever, 

ref. 211 
Parthenogenesis, artificial, in cells, ref. 

MattJieics, 106 
Pdssler on carcinoma of lung, ref. 480 
Pathological anatomy, 67 

histology, 67 

morphology, 67 

physiology, 67 

specimens, methods of preserving, 
51 
Pathology, characterization of, 67 

comparative, bibliography. 260 

comparative, importance of, 68 

general, 63 

general, introduction to, 65 

general, limitation of, 67 

special, 341 

special, limitation of, 67 
Pearce on bacteriology of scarlet fever, ref. 

250 
Pearls, epithelial, in epithelioma, 313 
Pediculus capitis, 139 
PelleiD on arsenic poisoning, ref. 324 
Pelvis of kidney, lesions of, 587 
Penis, calcification of. 651 

calculi in, 651 

cysts of, 651 

enlargement of, 650 

epispadias, 649 

examination of, 34 

fibrous plates in, 650 

hcemorrhage of, 650 

herpes of, 650 

hypospadias, 649 

inflammation of, 650 



804 



IXDEX. 



Penis, inflammation of glans of (see Bal- 
anitis), 650 

inflammation, syphilitic-, of, 650 

inflammation, tuberculous, of, 650 

injury of, 650 

malformations of, 649 

ossification of, 651 

paraphimosis of, 650 

phimosis of, 650 

smegma of, 650 

syphilis of, 650 

tulDerculosis of, 650 

tumors of, 650 
Pentastoma in liver, 559 
Pentastomum denticulatum in spleen, 380 

in lymph-nodes, 370 
Periarteritis, 412 

nodosa, 416 
Pericardial adhesions. 388 

fat, atrophy of, 394 

fibrous nodules, 390 

sac, obliteration of, 389 
Pericarditis, acute, 388 

bacteria of, 389 ' 

chronic, 389 

excitants of, 389 

exudative, 388 

fibrinous, 388 

infective, excitants of, 389 

purulent, 389. 

sero-fibrinous, 388 

suppurative, 389 

tuberculous, 390 
Pericardium, 387 

air in, 387 

calcification of, 389 

dropsy of, 387 

examination, post-mortem, of, 22 

haemorrhage of, 387 

inflammation of, 388 

injuries of, 387 

pneumonatosis of, 387 

tuberculosis of, 390 

tumors of, 390 
Perihepatitis, 552 
Perimetritis, 615 
Perinephritis, 588 
Periosteum, tumors of, 678 

lesions of, 663 
Periostitis, exudative, 663 

fibrous, 664 

ossifying, 664 

suppurative, 663 

syphilitic, 665 

tuberculous, 664 
Periphlebitis, 423 

chronic, 425 
Perisplenitis, 378 
Peritoneum, ascites of, 521 

cysts of, 526 

infection of, from intestine, 523 

inflammation of (see Peritonitis), 521 

inflammation, tuberculous, of, 523 

malformations of, 521 

parasites of, 526 

tumors of, 524 
Peritonitis, acute, 521 



Peritonitis, bibliography of, ref. 523 

bibliography of, ref. Bumm, 524 

cellular, 521 

chronic, 523 

excitants of, 523 

exudative, 522 

in typhoid fever, 206, 210 

suppurative, 522 

tuberculous, 523 
Pertussis, 251 
Petechise, 70 

Peterson on rectal strictures, ref. 516 
Petri's plates, 152 
Pever's patches, lesions of, in typhoid 

fever, 204, 366 
Pfeiffer on lysogenic action of antitoxic 

sera, 216 
Pfeiffer, Kitasato, and Canon on discovery 

of influenza bacillus, ref. 202 
Phagocytes, 116 

importance of, after haemorrhage, 70 
Phagocytosis, 116, 125 

a normal process, 124 

chemical nature of, 125 

in dead tissues, 92 

limitations of, 125 

relation of, to leucocytosis, 349 
Phar^^ngitis, " adenoids " in, 488 

catarrhal, 487 

croupous, 487 

diphtheritic, 487 

phlegmonous, 487 

tuberculous, 488 
Pharyngo-mycosis leptothrica, 201 
Pharynx, cysts of, 486 

diverticula of, 486 

examination of, post-mortem, and 
preservation of, 26, 42 

fistuhie of, 486 

inflammation of (see Pharyngitis), 487 

inflammation, tuberculous, of, 488 

malformations of, 486 

tumors of, 489 
Phimosis, 649, 650 
Phlebectasia, 422 
Phlebitis, 423 

acute, 424 

chronic, 425 

excitants of, 424 

infective, 424 

suppurative, 424 

syphilitic, 425 

tuberculous, 425 

uterine, 616 
Phleboliths, 422 

in thrombi, 73 
Phlegmon, 177 

gas-, 243 
Phloridzin diabetes, 335 
Phloroglucin for decalcification, 55 
Phosphorus necrosis of bone, 673 

poisonous action of, 323 
Phthisis, acute, 473 

chronic, 474 

pvdmonary, 471 

pulmonary (see Pulmonary Tubercu- 
losis), 471 



INDEX. 



805 



Plitliisis (see Tuberculosis, Pulmonary). 

473 
Physics, importance of, in pathology, 68 
Pia mater, method of preservation of, 16 

mater, post-mortem examination of, 
10 

mater cerebralis, characters of, 699 

mater cerebralis, cysts of, 708 

mater cerebralis, hajmorrhage of, 700 

mater cerebralis, hypersemia of, 700 

mater cerebralis, intlammation of (see 
Meningitis), 701 

mater cerebralis, inflammation, S3'ph- 
ilitic, of, 706 

mater cerebralis, inflammation, tuber- 
culous, of, 705 

mater cerebralis, oedema of, 700 

mater cerebralis, parasites of, 708 

mater, cerebralis, pigmentation of, 
701, 708 

mater cerebralis, tumors of, 706 

mater spinalis, blood content of, 709 

mater spinalis, bone in, 710 

mater spinalis, cartilage in, 710 

mater spinalis, h^iemorrhage of, 710 

mater spinalis, inflammation of, 710 

mater spinalis, parasites of, 710 

mater spinalis, tumors of, 710 
Picro-acid fuchsin, formulae and uses of, 

in staining, 60 
Pierson and Ravenel on aspergillus, ref. 156 
Pigment, anthracotic, in spleen, 373 

bacterial, 146 

hepatogenous, 88 

in blood, 351 

in ganglion cells, 733 

in liver, 543 

in lung, 461 

in sarcoma, 286 

in skin, 87, 88 

iron, in cells, ref. Arnold, 462 

melanotic, 88 

metabolic, 88 

normal and pathological, in the body, 
87 
Pigmentation, 87 

blood, 351 

hsemorrhagic, 70 

ha^matogenous, 87 

of adrenals, 385 

of liver, 543 

of lungs, 89, 461 

of pia mater cerebralis, 701, 708 

of skin from tattooing, 88 

of skin in Addison's disease, 332 

of spleen, 373 

of thyroid, 383 
Pineal gland, lesions of, 768 

gland, tumors of, 768 
Pin -worms, 135 
Pituitary body in acromegaly, 337 

body, lesions of, 768 

body, tumors of, 768 
Placenta, apoplexy of, 627 

cysts of, 628 

degeneration of, 627 

haemorrhage of, 627 



Placenta, infarction of, 627 

inflammation of (see Placentitis), 627 

lesions of, 627 

moles, hydatid, of, 628 

moles of, 628 

structure of, ref. Eden, 627 

syphilis of, 628 

tuberculosis of, 628 

tumors of, 628 
Placentitis, 627 
Plague, 242 

bacillus, 242 
Plasma cells, 103 

cells, differential staining of, with 
methylene blue, 60 

cells in granulation tissue, 119 

cells in tuberculous inflammation, 221 
Plasmodium malarice, 129, 252 
Pleomorphism in bacteria, 143 
Pleura, calcification of, 435 

cysts of, 437 

echinococcus of, 437 

haemorrhage, 433 

haemorrhagic exudates in, 433 

hydropneumothorax, 433 

hj^drothorax, 433 

inflammation of (see Pleuritis), 433 

lesions of, 433 

pyopneumothorax, 433 

tuberculosis of, 436 

tumors of, 437 
Pleural cavities, examination of, post- 
mortem, 21, 24, 25, 42 

cavities, post-mortem accumulation 
- of serum in, 25 
Pleurisy (see Pleuritis), 433 
Pleuritic fluid as culture medium, 152 
Pleuritis, 433 

acute, 433 

acute, excitants of, 434 

adhesions, 436 

chronic. 436 

emp3'emic, 435 

exudative, 433 

fibrinous, 433 

sero-fibrinous, 434 

sicca, 433 

suppurative, 435 

suppurative, excitants of, 436 

tul3erculous, 436 

tuberculous, diagnosis of, 437 

typhoid, Gordinier and Lartigau, ref. 
436 
Pneumococcus, 190 

meningitis, 195 

method of staining, 192 
Pneumonatosis of pericardium. 387 
Pneumonia, 449 

antitoxin, 191 

aspiration, 457 

broncho , 454 

broncho-, excitants of, 458 

broncho-, tuberculous. 468 

croupous, 450 

diphtheritic, 236 

experimental, ref. 459 

fibrinous, 450 



806 



INDEX. 



Pneumonia, haematogenous, 457 

hypostatic, 458 

influenza, 202 

interstitial, 460 

lobar, acute, 190, 450 

lobar, acute, excitant of (see Pneumo- 
coccus), 191 

lobar, complicating infections in, 453 

}obar, complicating lesions of, 452 

lobar, delayed resolution in, 453 

lobar, suppurative forms of, 454 

lobular, 454 

lobular, excitants of, 458 

organizing, 453 

purulent infiltration in, 454 

pysemic, 457 

suppurative, 454 

syphilitic, 479 

tuberculous, 462 

tuberculous, diffuse, 471 
Pneumonitis (see Pneumonia), 449 
Pneumonokoniosis, 89, 462 
Pneumonomykosis aspergillina, ref. 

Sayer, 156 
Pneumotoxin, 191 
Poikilocytes, 345 
Poisoning, food, 161 

method of examination in cases sus- 
pected of, 38 

opening of intestine in, 30 
Poisons, abrin, 327 

acid, arsenious, 323 

acid, carbolic, 326 

acid, carbonic, 328 

acid, hydrochloric, 322 

acid, hydrocyanic, 326 

acid, nitric, 321 

acid, oxalic, 322 

acid, sulphuric, 321 

acid, tartaric, 322 

aconite, 328 

alcohol, 326 

alkalies as, 322 

alkaline carbonates, 322 

alkaloidal, 328 

aloes, effects of, 325 

ammonia, 322 

arsenic, 323 

bibliography of, 328 

cantharides,"^ 325 
I carbonic oxide, 327 

cheese, 328 

chloral hydrate, 327 

chloroform, 327 

classification of, 330 

colchicum, 325 

colocynth, 325 

conium, 328 

copper, 325 

corrosive sublimate, 324 

croton oil, 325 

digitalis, 328 

elaterium, 325 

endogenous, 320, 328 

endogenous, histogenic, 329 

endogenous, microbic, 329 

ether, 327 



Poisons, exogenous, 320 

fish. 328 

forms of, 320 

fungi, 326 

gamboge, 325 

hellebore, 325 

ice-cream, 328 

ignorance of ultimate effects of, 330 

inorganic, 321 

insect, 327 

irritant, 325 

jalap, 325 

lead, 325 

lesions induced by, 320 

lobelia inflata, 328 

mercury, 324 

morphine, 326 

mussels, 328 

nature of, 320 

nitrobenzole, 326 

nux vomica, 327 

opium, 326 

Paris green, 324 

phosphorus, 323 

potash, 322 

potassium cyanide, 326 

potassium nitrate, 322 

potassium oxalate, 322 

ptomains, 328 

putrefactive substances, 328 

ricin, 327 

sausages, 328 

savin, 325 

scammony, 325 

Scheele's green, 324 

snake, 327 

soda, 322 

stramonium, 328 

strychnine, 327 

tartar emetic, 325 

turpentine, 325 

vegetable, 325 

venom, animal, 327 

veratria, 325 
Polar bodies in cells, 95 
Poliomyelitis anterior, 754 
Polychromatophilia, 357 
Polypi, fibrinous, of uterus, 610 

hairy, of pharynx, 489 

mucous, 281, 283 

nasal, 429 

of bronchi, 442 

of intestine, 519 

of mucous membranes, 280 

of pharynx, 489 

of urethra, male, 601 

of uterus, 617 
Popon on spinal-cord alterations in arsenic 

poisoning, 324 
Porencephalus, 767 
Portal vein, examination of, at autopsy, 32 

vein, lesions of., 537 
Portals of entry of micro-organisms, 160 
Posterior spinal sclerosis, 745 
Post-mortem accumulation of serum in 
pleural cavities, 25 

appearance of fractures, 8 



INDEX. 



807 



Post-mortem changes in abdomen, 20 
changes in hodj, 4 
changes in lungs, 25 
changes, relation of bacteria to, 5 
cooling of the body, 5 
cultures, 37 
decomposition. 5 

examination, closure of body after, 36 
examination, external inspection in, 4 
examination in arsenic poisoning, 324 
examination in cases of suspected poi- 
soning, 38 
examination in medico-legal cases, 37 
examination, internal, 8 
examination, method of making, 3 
examination, objects of, 3 
examination of abdomen, 19, 27 
examination of adrenals, 28 
examination of brain, 10, 41 
examination of head, 9 
examination of heart, 22 
examination of intestines, 30 
examination of kidneys, 27 
examination of larynx, 26 
examination of liver, 32 
examination of lungs, 25 
examination of new-born, internal, 4, 

41 
examination of pancreas, 33 
examination of pharynx, 26 
examination of pleural cavities, 24 
examination of solar plexus, 33 
examination of spinal cord, 17 
examination of spleen, 29 
examination of stomach and duode- 
num, 31 
examination of thoracic duct, 33 
examination of thorax, 19, 21 
examination of thyroid gland, 26 
heart clots, 23 
hypostasis, 4 
lesions of drowning, 46 
lesions of asphyxia, 44 
lividity, 4 

medico-legal cases, 38 
occurrence of rigor mortis, 6 
putrefaction, 5 
rise of temperature, 6 
specimens, bacterial examination of, 

37 
w^ounds, appearance of, 8 
Potash, poisonous action of, 322 
Potassium bichromate, use of, as a fixative 
in Miiller's fluid, 53 
cyanide, poisonous effects of, 326 
ferrocj^anide as test for iron in pig- 
ment, 87 
nitrate, poisonous action of, 322 
oxalate, poisonous action of, 322 
Potatoes as culture medium, 152 
Poucet and Berarcl on actinomyces, ref. 201 
Powers on carcinoma of branchial clefts, 

ref. 490 
Poynton and Payne on the excitant of 

rheumatism, ref. 252 
Pratt, ref. on histology of lobar pneumo- 
nia, 452 



Pratt on typhoid bacilli in skin, 212 

on vessels of heart, 404 
Preble on haemorrhage from oesophageal 

varices, ref. 550 
Preble and Hektoen on multiple neuroma, 

ref. 301 
Predisposition, hereditary, nature of, 164 

to infection, 163 
Pregnancy, extra-uterine, 640 
Preservation of pathological specimens, 51 

of specimens for gross demonstration 
and museums, 61 

of tissues, agents for, 52 

of tissues, importance of, 61 
Preservative fluids, importance of abun- 
dance of, 62 
Preventive inoculation, 171 

inoculation in Asiatic cholera, 216 

inoculation in bubonic plague, 242 

inoculation in rabies, 246 

inoculation in smallpox, 249 

inoculation in typhoid fever, 213 
Prickle cells in epithelioma, 313 
Primary degeneration of neurones, 744 
Proglottides of tapeworm, 131 
Progressive muscle atrophy, 687 
Protective mechanism of the body against 
bacteria, 159 

proteids, 125 
Proteids, protective, 125 

bacterial, 161 
Proteus vulgaris, 190 
Protozoa, 128 

methods of study, 130 

of malaria, 252 
Prostate, abscess of, 658 

atrophy of, 657 

calculi of, 659 

concretions in, 659 

cysts of, 659 

degeneration of, 657 

enlargement of, 657 

examination, post-mortem, of, 34 

hyperplasia of, 657 

hypertrophy of, 657 

inflammation of (see Prostatitis), 658 

inflammation, tuberculous, of, 650 

parasites of, 659 

tumors of, 659 
Prostatitis, 658 

tuberculous, 650 
Prudden, ref. on excitants of exudative 
pleuritis, 435 

on experimental cavity formation in 
animal tuberculosis, 478 

on local predisposition to infective en- 
docarditis, 407 

on multiple neuroma, 301 

on rhabdomyoma, 300, 529 
Prudden and Hodenpyl on the action of 

dead tubercle bacilli, 226 
Psammoma, 291, 699, 707, 709 
Pseudo-diphtheria, 186 
Pseudo-hermaphroditism, 649 
Pseudo-hypertrophy of muscle, 689 
Pseudo-leukaemia, 360 

liver lesions in, 554 



808 



INDEX. 



Pseudo-leukifmia, splenic lesions of, 380 
Pseudo-membrane of diplitlieria, 235 
Pseudo-membranous inflammation of mu- 
cous membranes, 186 
Psorospermiae, 129, 559 
Ptomains, bacterial, 146 

poisonous effects of, 328 
Puerperal fever, 615 
Pulmonary phthisis, 471 

tubercles, 464 

tuberculosis, 462 

tuberculosis, cavities in, 474 

tuberculosis, chronic, 474 

tuberculosis, concurrent infection in, 
476 

tuberculosis, diffuse, 471, 473, 474 

tuberculosis, distribution of lesions in, 
476 

tuberculosis, experimental, in animals. 
477 

tuberculosis, fibrous tissue, signifi- 
cance of, in, 476 

tuberculosis, focal, 464 

tuberculosis, nodular, 471 

tuberculosis, secondary lesions in, 475 
Purpura, 337 

hsemorrhagica, 70, 337 
Purulent inflammation, 123 
Pus, 115, 177 
Pustules, 176 

Putnam on encephalitis, ref. 753 
Putnam and Taylor on diffuse degeneration 

of spinal cord, ref. 751 
Putrefaction, relation of, to bacteria, 146 
Putrefactive substances, poisonous effects 

of, 328 
Pyaemia, cryptogenetic, 180 

lesions of, 180 

nature of, 179 

older views of, 179 

purpuric spots in, 337 
Pyelitis, 587 
Pyelo-nephritis, 587 
Pylorus, stenosis of, 493 
Pyogenic bacteria, 176. 181 
Pyopneumothorax, 433 
Pyosalpinx, 639 
Pyo-septicaemia, 180 

Quarter evil, 245 
Quinsy (see Tonsillitis), 488 

Rabies, 245 

diagnosis of, 247 
excitant of, 246 
lesions of, 245 

preventive inoculation in, 246 
virus of, 246 
Rachitis, 674 
Bainy on nerve lesions in diphtheria, ref. 

236 
Bamsay on malignant tumors of adrenals. 

ref. 386 
Ranula, 485, 528 
Rauschbrand, 245 

BaTenel and McCarthy on lesions of rabies, 
ref. 246 



Ray fungus, 200 

Rectocele vaginalis, 605 

Rectum, examination, post-mortem, of, 34 

lesions of. 
Red blood cells, destruction of, 87 
Beed on excitant of smallpox, ref. 249 

on focal lesion in liver . in typhoid 
fever, etc., 209 
Beed and Carroll on the excitant of yellow 

fever, 248 
Beed, Carroll, and Agramonte on the mos- 
quito in j^ellow -fever infection, ref. 248 
Regeneration, 94 

of blood, 105 

of blood-vessels, 104 

of bone, 105 

of cartilage, 105 

of cells, characters and limitations of, 
98 . 

of cells, conditions which incite, 105 

of cells, Fnerst, ref. 273 

of connective tissue, 102 

of epithelium, 101 

of liver, 102 

of lost parts in lower animals, 99 

of mucous membranes, ref. Cornil and 
Cnrnot, 101 

of muscle tissue, 100 

of nerve tissue, 99 

of nerve tissue, ref. Barker, 739 

of neuroglia, 100 

of special tissues, 99 

physiological, of tissue, 94 

significance of cell types in, 99 

tissue types in which it is most com- 
plete, 99 
Beinhacli on colloid substance and struma, 

ref. 383 
Beinehoth and Kohlliardt on cooling as pre- 
disposing to infection, ref. 460 
Beisman on Meckel's diverticula, ref. 504 
Relapsing fever, 241 
Renal calculi, 590 
Benan on aspergillosis, ref. 156 
Reparative inflammation, 117 
Repair of injury by first intention, 108 
Replacement hyperplasia in nerve tissue, 

740 
Reproductive organs, female, 602 

organs, male, 649 
Resolution after inflammation, 115 
Respiratory system, 429 

system, sudden death from lesions of, 
50 
Reversion in liver cells, 549 

of cells, importance of, 66 
Rhabdomyoma, 299 

of heart, 410 

of parotid, 529 

of testicles, 656 
Rhabdonema strongyloides. 138 
Rheumatism, 252, 683 
Rhexis, haemorrhage by, 69 
Rhinitis, 429 
Rhinoscleroma, 235 
Rhizopoda, 128 
Bibbert, ref. on appendicitis, 518 



INDEX. 



809 



Ribbert on hypothesis of origin of tumors, 
ref. 273 

on inflammation and regeneration of 
lymph-nodes, 366 
Rlcin in toxiTemia, ref. Flexner, 178 

toxic action of, 161, 327 
Bicker on pathogenic yeasts and moulds, 

ref. 158 
Rickets (see Rachitis), 674 

lymphatic constitution in, 337 
Rieder on leucocytosis, ref. 350 
Ries on salpingitis, ref. 639 
Kigor mortis. 6, 7 
Ritclde, ref. on bacteria in bronchitis, 439 

on cystic kidnej", 589 
Rixford and Gilclirist on protozoan infec- 
tion of skin, ref. 129 
Robinson on tonsillar calculi, ref. 488 
Roger and Gamier on tuberculosis of thy- 
roid, ref. 383 
Rolleston and Grofton-AtMns on pyloric 

stenosis, ref. 493 
Rolleston and Hague on congenital cirrho- 
sis, ref. 551 
RornanoirsTcV s stain for malarial blood, 260 
Rupture of arteries, 410 

of bladder, urinary, 594 

of heart, 393 

of intestine, 505 

of liver, 535 

of muscle, 691 

of oesophagus. 490 

of spleen, 372 

of stomach, 493 

of urethra, 600 

of uterus, 609 

of veins, 423 
Russell on combined system degenerations, 
ref. 750 

on ovarian cj^sts, ref. 636 
Rutimeyer on Friedreich's ataxia, ref. 751 

Saccharomyces, 156 

Sacerdotti on hvpertroph}' of kidney, ref. 

564 
Sailer on transplantation of tumors, ref. 267 
Salamanders, regeneration of lost parts in, 

99 
Salivary glands, lesions of, 210, 526 

glands, tumors of. 528 
Salpingitis, catarrhal, 639 

suppurative, 639 

syphilitic, 639 

tuberculous, 639 
Salt solution for studying bacteria, 149 

solution for studying fresh tissues, 15 
Saltpetre, poisonous action of. 322 
Salvetti on rickets, ref. 674 
Sanarelli on the yellow-fever bacillus, ref. 

248 
Saprophytic bacteria, 147 
Sarcina, 142 
Sarcoma, 283 

adeno-, 291 

alveolar, 289 

angio-, 289 

characters of. 283 



Sarcoma, chondro-, 291 

cysto-, 290 

deciduo-cellulare, of uterus, 626 

endothelial. 291 

tibro-, 285 

fusocellulare, 285 

ffiant-celled, 286 

glio-, 286 

lipo-, 291 

Ivmpho-, 286 

melano-, 286 

mixed, 290 

myeloid. 286 

myo-, 291 

myxo-, 290 

of adrenals, 386 

of arteries, 421 

of bladder, urinary, 597 

of bone, 680 

of bronchi, 442 

of brain, 765 

of dura mater cerebralis, 698 

of dura mater spinalis, 709 

of ependvma, 714 

of heart, '410 

of intestine, 519, 520 

of kidney, 590 

of larynx, 432 

of liver, 556 

of lung, 480 

of lymph-nodes, 370 

of mamma, 645 

of mamma, male, 660 

of muscle, 693 
' , of nerves, 767 

of nose, 429 

of oesophagus, 492 

of ovaries, 632 

of parotid. 528 

of pericardium, 390 

of peritoneum. 524 

of pharynx, 490 

of pia mater cerebralis, 708 

of pleura, 437 

of prostate, 659 

of spinal cord, 765 

of spleen, 380 

of stomach, 501 

of submaxillary glands, 528 

of testicles, 656 

of thymus, 381 

of thyroid, 384 

of ton2:ue, 485 

of tonsil, 490 

of uterus, 619 

of vagina, 606 

of veins, 425 

of vulva, 604 

osteo-, 288 

retroperitoneal, 524 

round-celled, 285 

spindle-celled, 285 
Sarcoptes homiuis, 139 
Sausage poisoning, 328 
Savin, poisonous effects of, 325 
Sayer on pneumonomykosis aspergillina, 
ref. 156 



810 



IITDEX. 



Scagliosi on lesion of tlie heart in diph- 
theria, ref. 236 
Scammony, poisonous effects of, 325 
Scariatina, 250 
Scariet fever, 250 
Scars, permanence of, 8 
Schanzes microtome, 58 
Scheele's green, poisonous effects of, 324 
Schizomycetes, 141 
ScMegel on actinomycosis, ref. 201 
Schmidt, ref. on amyloid tumors, 485 

on bone pathology, 682 
Schvltz on cj^sts of the stomach, 503 
Schidtze on descending degeneration, 743 
Schulze on branching forms of B. tubercu- 
losis, 222 
Scirrhous carcinoma of mamma, 646 
Scirrhus carcinoma, 317 
Sclerose en plaque, 759 
Sclerosis, amyotrophic lateral, 745 

multiple, of brain and cord, 759 

multiple, of spinal cord, 760 

of arteries, 412 

of brain, 758 

of spinal cord, 759 
Scolex of tapeworms, 131 
Scorbutus, 70, 336 
Scrofula, bibliography of, ref. Cornet, 368 

lymph-nodes in, 367 
Scrotum, cysts of, 651 

dermoid cysts of, 651 

elephantiasis of, 651 

lesions of, 651 

tumors of, 651 
Scudder on mammary tuberculosis, ref. 643 
Scurvy, 70, 336 
Sebileau on orchitis, ref. 656 
Secretions, internal, 329 
Seven-day fever, 241 
Section cutting, 55, 58 
Sections, frozen, methods for, 51 
Selective filtration in formation of serum, 

112 
Semilunar ganglia, examination, post- 
mortem, of, 33 
Seminal vesicles, concretions in, 657 

vesicles, cysts of, 657 

vesicles, lesions of, 657 

vesicles, tumors of, 657 
Senility, changes in, Miilihnann, ref. 87 
Septic intoxication, 161 
Septicaemia, bacteria in blood in, 181 

diphtheritic, 237 

hsemorrhagic, 243 

lesions of, 179, 180 

nature of, 164 

typhoid, 212 
Septico-pya^mia, 180 
Sequestrum of dead bone, 672 
Serous apoplexy, 722 

infiltration, 84, 691 

inflammation, 123 
Serum, action of, in inflammation in dilut- 
ing poisons, 126 

anti-plague, 243 

antitoxic, lysogenic action of, 216 

blood-, as culture medium, 152 



Serum, formation of, in inflammation, 
111 

germicidal powers of, 125 

in cerebral meninges, 10 
Serum-therapy, 171 

in diphtheria, 238 
ShaiD on chylous ascites, ref. 521 
Sherrington on escape of bacteria with se- 
cretions, ref. 160 
Ship fever, 247 

Shoher on malpositions of colon, ref. 503 
Siderosis of lung, 462 
Silherschmidt on peritonitis, ref. 523 
Silver, pigmentation of skin from, 88 
Simon on blood, ref. 351 
Sinus pocularis, dilatation of, 601 
Sittmannon elimination of bacteria by the 

kidney, ref. 577 
Size and weight of organs, tables, ref. 

Vierordt, 8 
Skull, method of opening of, 9, 41 
Smallpox, 249 

Immunity in, 172, 249 
Smegma, 650 

bacillus, 225, 229 
Smith, A. H., on carcinoma of thoracic 

duct, ref. 426 
S?nith, Theobald, ref. on adaptation of path- 
ogenic bacteria to different animal 
species, 169 

on bacilli of bovine tuberculosis, 225 
Snails, regeneration of lost parts in, 99 
Snake venom, ref. to Langman, 327 
Soda, poisonous action of, 322 
Sodium chloride for study of fresh tissues, 

51 
Sodre on beri-beri, ref. 251 
Soft chancre, 197 
Soil, bacteria in, 147 
Sokoloff on adeno-carcinoma of liver, ref. 

555 
Solar plexus, post-mortem examination of, 

33 
Somatochromes, 731 
Soor, 483, 485 

Spengler on concurrent infection in tuber- 
culosis, ref. 228 
Spermatocele, 653 
Spider cells, 297 
Spina bifida, 717 
Spinal cord, apoplexy of, 725 

cord, artefacts of, 717 

cord, asymmetry of, 716 

cord, blood-vessels of, 720 

cord, blood-vessels of, lesions of, 730 

cord, cysts of, 766 

cord, degeneration, ascending, of, 743 

cord, degeneration, descending, of, 742 

cord, degeneration, systemic, of, 740 

cord, distortions of, 716 

cord, embolism of, 729 

cord, examination, post-mcrtem, of, 
17, 42 

cord, haematomyelia, 726 

cord, hsematomyelopore, 727 

cord, haemorrhage of, 725 

cord, hardening, methods of, 19 



INDEX. 



811 



Spinal cord, inflammation of (see Myelitis), 
753, 760 

cord, inflammation, chronic, 758 

cord, injuries of, 718 

cord, location of lesions of, 18 

cord, malformations of, 715 

cord, methods of study, 769 

cord, post-mortem alterations in blood 
and fluids of, 17 

cord, sclerosis of, 759 

cord, staining methods for, 769 

cord, sj^philis of, 763 

cord, thrombosis of, 729 

cord, tuberculosis of, 762 

cord, tumors of, 765 

nerve roots, anomalies of, 716 
Spirals, Curschmann's, 440 
Spiremes in cell division, 95 
Spirilla, 141 
Spirillum, 141 

cholercT Asiaticse, 214, 216 

fever, 241 

sputigenum, 217 

tyrogenum, 217 
Spirochaete Obermeieri, 241, 381 
Spleen, 371 

absence of, 371 

accessory, 30, 371 

amyloid, 371 

ausemia of, 373 

atrophy of, 372 

bacteria in, 381 

capsule, inflammation of, 378 

character of, 371 

circulatory disturbances in, 373 

congestion of, 374 

degeneration, amyloid, of, 372 

displacements of, 371 

double, 371 

embolism in, 374 

enteroptosis of, 27 

examination, post-mortem, of, 29, 43 

haemorrhage of, 372 

hardening of, 30 

hyperaemia of, 374 

hyperplasia, endothelial, of, 379 

hyperplasia in leukaemia and pseudo- 
leukaemia, 380 

hyperplasia of, 375 

induration of, 376 

infarction of, 210, 374 

inflammation, acute, of, 375 

inflammation, chronic, of, 376 

inflammation, syphilitic, of, 377 

inflammation, tuberculous, of, 377 

leukaemic lesions in, 380 

malarial, 377 

malformations of, 371 

parasites of, 380 

pigmentation of, 373, 377 

pseudo-leukaemia, lesions of, 380 

role of, in infection, ref. Courmont 
and Duffau, 376 

rupture of, 372 

"sago," 372 

situation of, 29 

size of, 29 



Spleen, structure of, 29 

suppuration of, 376 

syphilitic, 377 

thrombosis in, 375 

transposition of, 371 

tumors of, 380 

weight of, 29 

wounds of, 372 
Splenic fever, 197 

tumor, acute, 375 
Splenitis, 375 

peri-, 378 
Splenomegaly, 379 
Spores of bacteria, 143, 144, 145 
Sporiangium of moulds, 156 
Sporozoa, 129 

of malaria, 252 
Sporozoites of malarial parasites, 257 
Spotted fever, 247 
Sputum, numbers of bacilli in tuberculous, 

227 
Staining, methods for, 59 
Staphylococcus cereus albus, 183 

cereus flavus, 183 

epidermidis albus, 183 

pyogenes albus, 183 

pyogenes aureus, bibliography of, 
183 

pyogenes aureus, character of, 181 

pyogenes aureus, effects of, in body, 
182 

pyogenes aureus, modes of distribu- 
tion of, 183 

salivarius pyogenes, 183 
Status lymphaticus, 337 
Steele on retroperitoneal sarcoma, ref. 525 
Stenosis of oesophagus, 491 
Stepanow's method for rapid celloidin em- 
bedding, 56 
Sterilization of bacteria, 144, 145 
Stern on tumors in childhood, ref. 319 
Sternlerg, discovery of pneumococcus by, 
191 

on the 3^ellow-fever bacillus, ref. 248 
Stokes on vaginal cysts, ref. 606 
Stomach, atrophy of, 494 

bibliography of lesions of, ref. Thorel, 
503 

cadaveric alterations in, 493 

changes in position of, 21 

contents of, after drowning, 48 

cysts of, 503 

degeneration of, 494 

dilatation of, 500 

erosions, haemorrhage of, 500 

etat mamelonne of, 496 

examination of, post-mortem, 31 

foreign bodies in, 503 

haemorrhage of, 494 

haemorrhagic erosions of, 500 

hair balls in, 503 

hardening and preservation of, 32 

inflammation of (see Gastritis), 495 

inflammation, syphilitic, of, 498 

inflammation, tuberculous, of, 498 

injuries of, 493 

malformations of, 493 



812 



INDEX. 



Stomach, micro-organism of, ref . Weiss and 
Coyon, 497 

poisons, action of, on, 497 

position of, 21 

rupture of, 493 

tuberculosis of, 498 

tumors of, 500 

ulcers of, 498 
Stomatitis, aphthous, 483 

catarrhal, 482 

chronic, 483 

croupous, 483 

gangrenous, 483 

parasitic, 483 

plilegmonous, 483 

syphilitic, 484 

tuberculous, 483 

ulcerative, 483 
Stramonium, poisonous effects of, 328 
Strangulation, 45 

post-mortem marks of, 7 
Straus on tuberculosis, ref. 230 
Strawberry marks, 303 
Streptococcus, 142 

anaerobic, 184 

antitoxin of, 185 

bibliography of, 185 

brevis, 184 

conglomeratus, 184 

erysipelatis, 185 

longus, 184 

pyogenes associated with B. diph- 
therige, 237 

pyogenes, characters of, 183 

pyogenes, effects of, in body, 184 
Streptothrix, actinomyces, 143, 200 

bacilli, 142 

in lungs, 201 

madurse, 201 
Strictures of appendix, 517 

of urethra, 599 
Stroebe on tuberculosis of the aorta, ref. 

417 
Strong on capsule bacilli, ref. 189 
Strongylus gigas, 136, 592 
Struma of adrenals, 386 

of thyroid, 383 

suprarenalis lipomotosa, 386 
Strychnine, poisonous effects of, 38, 327 
Subinfection, ref. Adami, 160 
Sublingual gland, lesions of, 528 
Submaxillary gland, lesions of, 210, 527, 

528 
Sudden death, 49 
Suffocation, 44 
Suggillations, 70 
Sunstroke, 335 
Suppuration, 120 

bacteria of, 181, 187 

excessive, damage by, 126 
Suppurative inflammation, 123, 175 
Supra-arterial epicardial fibroid nodules, 

390 
Suprarenal bodies (see Adrenals), 385 

capsules (see Adrenals), 385 

capsules, examination, post-mortem, 
of, 28 



Suprarenal glands, relation of, to Addi- 
son's disease, 332 
Sutton on tumors, ref. 319 
Swabs, cotton, for collecting culture mate- 
rial, 155 
Symbiosis in bacteria, 148 
Syncope, death from, in drowning, 46 

death, sudden, from. 50 
Syncytioma of uterus, 626 
Synovial membranes, lesions of (see Arthri- 
tis), 683 
Syphilis, 232 

blood-vessels, lesions in, ref. Ahramow, 
418 

congenital, of bone, 671 

haemorrhage in, 71 

lesions of, 232 

of adrenals, 386 

of arteries, 417 

of bone, 665, 666. 670 

of dura mater cerebralis, 698 

of Fallopian tubes, 639 

of heart, 406 

of intestine. 508 

of kidney, 587 

of larynx, 432 

of liver, 551 

of lung, 479 

of lymph-nodes, 368 

of lymph-vessels, 427 

of mamma, 643 

of meninges, 706 

of mouth, 484 

of nervous system, 763 

of nose, 429 

of ovaries, 631 

of penis, 650 

of pia mater cerebralis, 706 

of placenta, 628 

of spleen, 377 

of stomach, 498 

of testicle, 655 

of thymus, 381 

of urethra, 601 

of uterus, 614 

of vagina, 606 

of veins, 425 

of vulva, 603 
Svringomyelia, 766 

false, '727 
Systemic degeneration of neurones, 740 

Tabes dorsalis, 745 
Taenia cucumerina, 134 

echinococcus, 132 

flavopunctata, 134 

madagascariensis. 134 

mediocanellata, 132 

nana, 134 

solium, 131 
Tapeworms, 131 

Tartar emetic, poisonous effects of, 325 
Tattoo marks, appearance of, after death; 

8 
Tavel and Lanz on peritonitis, ref. 523 
Taylor on fatty degeneration, ref. 80 

on poisons, ref. 328 



IXDEX. 



813 



Teratoma, 269, 276 

of liver, 557 

of mediastinum, 481 

of ovary, 637 

of pineal gland, 768 

of scrotum, 651 

of testicle, 657 
Terminal infection, 165 
Testicles, abscess of, 653 

absence of, 651 

atrophy of, 653 

cryptorchismus, 652 

cysts of, 656 

examination, post-mortem, of, 34 

inflammation of (see Orchitis), 653 

inflammation, syphilitic, of, 655 

inflammation, tuberculous, of, 654 

malformations of, 649, 651, 652 

parasites of, 657 

tumors of, 656 

weight of, 34 
Tetano-toxin, 239 
Tetanus, 239 

antitoxin, 240 

bacillus, 239 

group of bacilli, 240 
Tluidier on melanuria, ref. 286 
Thayer on malarial nephritis, ref. 577 
TTiayer and Hewetson on malaria, ref. 259 
Theisen on phar^^ngeal tuberculosis, ref. 

488 
Thionin, use of, in staining malarial blood, 

259 
Thmna, ref. on arterio-sclerosis, 416 

on hypertrophj^ 564 

on inflammation, 126 

on malformations of brain, 715 

on mitotic figures, 98 
Thoma's microtome, 58 
Thomas and Hibbard on lesions of the 

heart in diphtheria, ref. 236 
Thoracic duct, examination, post-mortem, 
of, 33 

duct, obstruction of, 426 
Thorax, post-mortem examination of, 19, 

21,42 
Thorel, ref. bibliography of intestinal 
lesions, 520 

on lesions of salivary glands, 528 

on regeneration in renal epithelium, 
565 
Thread worms, 135 
Thymus, hypertrophy of, 381 
Thyroid, 382 

accessory, 382 

atrophied, in myxoedema, 331 

circulatory disturbances in. 383 

cretinism in lesions of, 331 

degenerations in, 382 

examination and preservation of, 26 

haemorrhage of, 383 

hypersemia of, 383 

hyperplasia of, 383 

hvpersecretion of, and exophthal- 
'mus, 323 

inflammation of, 383 

malformations of, 882 



Thyroid, myxoedema, relation of, to, 331 

parasites of, 385 

pigmentation of, 383 

struma of, 383 

syphilis of, 383 

tuberculosis of, 383 

tumors of. 384 

weight of, in infants, 42 
Thrombi, conditions favoring, 72 

hyaline, 75 

in pyaemia, 181 

in typhoid fever, 207 

lamellated, 74 

mixed, 73 

occluding, 72 

organization of, 73, 121 

organized, in heart, 399 

parietal, 72 

purulent, 78 

red, 78 

septic, 73 

significance of, 75 

simple, 78 

softening of, 78 

wiiite, 78 
Thrombosis, globular, of heart, 899 

nature of, 72 

of adrenals. 385 

of brain, 727, 729 

of coronarj" arteries, 402 

of dura mater cerebralis, 695 

of heart, 898, 399 

of heart valves, 409 

of kidney, 565 
- of portal vein, 537 

of spinal cord, 729 

of splenic vein, 375 

of vena cava, 428 

pulmonary, 445 

venous, 428 
Thrombus (see Thrombi and Thrombosis) 
Thrush, 488 
Thymus, 381 

accessory, 381 

atrophy of, 881 

haemorrhage of, 881 

hyperplasia of, 381 

hyperplasia of, in Hodgkin's disease, 
360 

inflammation of, 881 

involution of, 381 

malformations of, 881 

period of formation of, 89 

persistent, 881 

size of, in infants, 42 

syphilis of, 381 

tuberculosis of, 881 

tumors of, 381 

weight of, in infants, 42 
Thyroidism, experimental, ref. Cunning- 
ham, 331 
Thyroiditis, 388 
Tic douloureux, lesions in, 761 
Tidy, Legal Medicine, ref. 7, 48 
Tilger on pancreatic cysts, ref. 588 
Tizzoni on adrenal removal, ref. 383 
Tongue, amyloid tumors of, 485 



814 



IlS^DEX. 



Tongue, cysts of, 485 

ini3ammation of, 485 

malformations of, 484 

tumors of, 485 
Tonsillitis, chronic. 488 

excitants of, 488 

exudative, 488 

follicular, 488 

phlegmonous, 488 

suppurative, 488 
Tonsils, anatomy of, ref. Hodewpyl and 
Packard, 488 

as portals of entry for micro-organ- 
isms, ref. t\ Sclieiher. 488 

bibliography of, ref. Ullmann, 489 

bone and cartilage in, 490 

calculi of, 488 

hyperplasia of, 210, 488 

hypertrophy of, 488 

inflammation of (see Tonsillitis), 488 

lesions of, 488 

tumors, maliguant, of, Housell and 
Newman, ref. 490 
Tooth on secondary degeneration of spinal 

cord, ref. 743 
Toxaemia, 178 

bacterial, 161 

ganglion-cell lesions in, 737 
Toxalbumin intoxication, ref. Flexner, 162 
Toxalbumins, 146, 161 
Toxalbumoses, 161 
Toxins, bacterial, 146, 161 

effects of, on neurones, 737 

of diphtheria, 238 

of tetanus, 239 
Trachea, examination of, in infants. 42 

lesions of, 432 

lymph-nodes of, 442 

malformations of, 430 

tumors of, 432 
Transudate, composition and nature of, 72 
Transudates as culture media, 152 
Transudation, 71 
Trematoda, 130 
TrepinsM on tabes, ref. 749 
Trichina spiralis, 136 

spiralis in blood, 354 

spiralis in lymph -nodes, 370 

spiralis in muscle, 694 
Trichocephalus dispar, 136 
Trichomonas vaginalis, 130, 606 
Trichophyton tonsurans, 157 
Tropical dysentery, 511 
Tubal pregnancy, 640 
Tubercle, diffuse, 221 

granulum, 218 

bacillus, action of, on living tissues, 
217, 218 

bacillus, bacilli resembling, 229 

bacillus, characters of, 222 

bacillus, dead, action of, 225 

bacillus, varieties of, 225 

tissue, 218 
Tubercles, 217 

conglomerate, 218 

healed, of lungs, 467 

lymphoid, 221 



Tubercles, miliary, 217, 218, 464 

miliary, characters of, 218 

morphological forms of, 221 

polyhedral-celled, 221 

solitary, of brain, 762 

structure of, 218 
Tuberculin, 225 
Tuberculosis, 217 

animal, 227 

association with diphtheria, ref. 237 

avian, bacilli of, 225 

bibliography of, 229 

cardiac, 409 

children, in, ref. Guilirie, 228 

complex factors involved in, 226 

concurrent infection in, 228 

diffuse, 218 

distribution of lesions in, 228 

exudative forms of, 222 

focal, of lung, 464 

frequencv of, in man and lower ani- 
mals, 227 

healing in, 226, 227, 467, 476 

human, 227 

hyperplastic, of ileo-C£ecal region, 515 

localized, 217 

mammalian, bacilli of, 225 

miliary, 218 

miliary, acute, origin of, ref. Benda, 
466 

mixed infection in, 228 

morphology of, 217 

number of bacilli in lesions of, 227 

of adrenals, 385 

of arteries, 417 

of bladder, 596 

of bone, 665, 666, 670 

of dura mater cerebralis, 698 

of dura mater spinalis, 709 

of endocardium, 409 

of Fallopian tubes, 639 

of heart, 406 

of heart thrombus, 399 

of intestine, 507 

of joints, 684 

of kidney, 586 

of larynx, 431 

of liver, 552 

of lungs, 462 

of lymph -nodes. 366 

of lymph-vessels, 427 

of mamma, 642 

of meninges, 705 

of mouth, 483 

of nervous system, 762 

of nose, 429 

of oesophagus, 492 

of ovaries, 631 

of parotid, 528 

of penis, 650 

of pericardium, 390 

of peritoneum, 523 

of pharynx, 488 

of pia mater cerebralis, 705 

of pia mater spinalis, 710 

of placenta, 628 

of pleura, 436 



IXDEX. 



815 



Tuberculosis of prostate. 658 
of seminal vesicles. 657 
of skin, lupus, 229 
of spleen, 376 
of stomach. 498 
of testicle. 654 
of thymus, 381 
of urethra. 601 
of uterus, 613 
of vagina. 606 
of veins, 425 
of vulva, 603 

portals of entry of bacilli in, 228 
predisposition to, 218 
pulmonary, 462 
pulmonary, cavities in, 474 
pulmonarj', chronic, 474 
pulmonary, concurrent infection in, 

476 
pulmonary, distribution of lesions in. 

476 
pulmonary, experimental, in animals 

477 
pulmonarj^, fibrous tissue, significance 

of, in. 476 
pulmonar}^, miliary, chronic, 468 
pulmonary, nodular, 471 
pulmonary, secondarj^ lesions in, 475 
repair in, 220 
resemblance of lesions of, to svphilis. 

233 
susceptibility of man and animals to. 

227 
Tuberculous bronchiectasia, 471 
broncho-pneumonia, 468 
pachymeningitis, 698 
pneumonia, 462 
Tumors, 261 

alveolar, 306 

amyloid, of larynx and trachea, 432 
amyloid, of tongue, 485 
anaplasia in, 273 
atypical growth in, 263 
autononi}' of, 262 
bacteria as excitants of, 270 
■ benign, 265 

bibliography of, 319 
blood-vessels in, 268 
cachexia of, 265 
cells of, characteristics of, 266 
changes in adjacent parts by, 264 
characters, general, of, 261, 262 
childhood, in, ref. to Stern, 319 . 
classification of, 274 
classification, LiibarscTi's, 276 
coccidia as excitants of, 270 
combinations of, 275 
complex, 275 
complex congenital, 276 
congenital, 276 
cj'stic, 277 

degenerations in, 263 
destructive processes in, 263 
diagnosis, elements of, in, 266 
diathesis of, 266 
dissemination, modes of,, 264 
dvscrasia of, 266 



Tumors, embolic, 264 
endothelial, 291 
epithelial, 305 
etiolog}' of, 267 
etiology of, age. 267 
etiology of, Cohnheim's hypothesis, 

269 
etiology, complexity of problem of, 

272 
etiology of, heredity, 269 
etiology of, local predisposing factors, 

268, 269 
etiology of, micro-organisms, 270 
etiolog'y of, sex, 267 
fat, 29^5 

formative cell-stimulus in, 272 
generalization of, 264 
grafts of, 266 
groups of, 274, 276 
hcemorrhage in, 263 
histogenetic classification of, 274 
importance of animal species in grafts 

of, 267 
inflammation in, 263 
lesions simulating, 278 
lymph-vessels in, 263 
maintenance of cell types in, 264 
malignancy of, 265 
metastasis of, 264 

micro-organisms as excitants of, 270 
mitosis in, 263 
mixed, 275 

modes of growth and extension of, 264 
multiple, 264 
necrosis in, 263 
' nerves in, 263 
of adrenals, 386 
of appendix vermiformis, 520 
of arteries, 421 
of bladder, 597 
of bone, 678 
of brain, 764 

of breast (see Mamma), 643 
of bronchi, 442 
of clitoris, 603 

of dura mater cerebralis, 698 
of dura mater spinalis, 709 
of ependyma, 714 
of Fallopian tubes, 689 
of gall bladder, 561 
of gall ducts, 561 
of heart, 410 
of intestine, 518 
of joints, 685 
of kidney, 590 
of labia, ^603 
of larynx, 432 
of liver, 554 
of lungs, 480 
of lymph-nodes, 370 
of lymph-vessels, 427 
of mamma, 643 
of mediastinum, 481 
of mouth, 484 
of muscle, 693 
of nerves, 767 
of nose, 429 



816 



INDEX. 



Tumors of o'sopbagus, 492 

of omentum, ref. Giannetiasio, 504 

of ovaries, 631 

of pancreas, 532 

of parotid, 528 

of jDenis, 650 

of pericardium, 390 

of periosteum, 678 

of peritoneum, 524 

of pharynx, 489 

of pia mater cerebralis, 706 

of pia mater spinalis, 710 

of pineal gland, 768 

of pituitary body, 768 

of placenta, 628 

of pleura, 437 

of prostate, 659 

of salivary glands, 528 

of scrotum, 651 

of seminal vesicles, 657 

of spinal cord, 765 

of spleen, 380 

of stomach, 500 

of submaxillary glands, 528 

of testicle, 656 

of thymus, 381 

of thyroid, 384 

of tongue, 485 

of trachea, 432 

of umbilicus, 526 

of urethra, male, 601 

of uterus, 616 

of vagina, 606 

of veins, 425 

of vulva, 603 

parasites as excitants of, 270 

protozoa as excitants of, 270 

rapidity of growth of, 263 

recurrence of, 265 

Ribbert's hypothesis of the origin of, 
273 

sacral, ref. Borst, 276 

shape of, 263 

significance, original, of, 261 

tissue types in, 263 

transplantation of, 266 

types of, 274, 276 

types, mixed, 275 
Tilrk on leucocytosis, ref. 350 
Turner on tumor of pineal gland, ref. 768 
Turpentine, poisonous effects of, 325 
Typhoid bacillus, characters of, 204 

bacillus, colon bacillus, relation of, to, 
214 

bacillus, distribution of, in body, 212 

bacillus, extra-intestinal lesions in- 
duced by, 210 

bacillus, metliods of staining, 214 

bacillus, pyogenic powers of, 213 

bacillus, resistance to cold, 213 

epidemics from milk and water pollu- 
tions, 213 

fever, 203 

fever, concurrent infection in, 212 

fever, hyperplasia of Peyer's patches 
in, 366 

fever, lesions of, in lymph -nodes, 208 



Typhoid fever, lesions of spleen in, 208 
fever, lesions, primary, of, 204 
fever, lysogenic action of antitoxic 

serum of, 217 
fever, lymphocytosis in, 349 
fever, modes of infection in, 213 
fever, preventive inoculation in, 213 
fever, secondary lesions of, 210 
fever, secondary lesions of, in bone, 

211 ' 
fever, secondary lesions of, in circula- 
tory organs, 210 
fever, secondary lesions of, in diges- 
tive organs, 210 
fever, secondary lesions of, in genito- 
urinary organs, 211 
fever, secondar}"^ lesions of, in nervous 

system, 211 
fever, secondary lesions of, in respira- 
tory organs, 211 
fever, secondary lesions of, suppura- 
tive, 211 
fever, septicsemic forms of, 212 
ulcers, 206 
Typhotoxin, 204 
Typhus fever, 247 
recurrens, 241 
Tyrosin in necrotic tissue, 90 

Ulceration, 90 

of bone, 673 
Ulcers, healing of, by granulation tissue, 
121 

of bone, 673 

of intestine, 508 

of mouth and pharynx in typhoid 
fever, 210 

of stomach, 498 

of uterus, 610 

phagedenic, of uterus, 610 

syphilitic, of penis, 650 

typhoid, characters of, 206 
TJlrich on renal lipoma, ref. 590 
Umbilical cord, changes in, after birth, 
40, 41 

cord, strangulation by, marks of, 41 

tumors, ref. Giannettasio, 504 

tumors of, 526 
Urachus, malformation of, 593 
Ureter, lesions of, 587 
Ureteritis, 587 
Urethra, examination, post-mortem, of, 34 

male, cysts of, 601 

male, dilatations of, 599 

male, haemorrhoids of, 601 

male, inflammation of (see Urethritis), 
600 

male, invagination of, 600 

male, malformations of, 599 

male, malpositions of, 599 

male, obstruction of, 599 

male, perforation of, 600 

male, prolapse of, 600 

male, rupture of, 600 

male, sinus pocularis, dilatation of, 601 

male, strictures of, 599 

male, syphilis of, 601 



INDEX. 



817 



Urethra, male, tumors of, 601 

male, wounds of, 600 
Urethritis. 600 

syphilitic, 601 

tuberculous, 601 
Urinary organs, 564 
Urine, collection of, at autopsy, 34 

typhoid bacilli in, 212 
Uterus, absence of, 606 

atrophy of, 610 

bacteria in infections of, ref. Wads- 
worth, 616 

bacteria of, ref. 611 

bifid, 607 

cervix, stenosis of, 607 

congestion of (see Hyperemia of), 609 

cysts of. 627 

degenerations of, 610 

dilatation of, 607 

displacements of, 608 

double, 607 

elevation of, 608 

endometritis, 611 

enlargement of, 607 

examination, post-mortem, of, 35 

flexion of, 608 

hgematocele of, 610 

hsematoma, polypoid, of, 610 

haemorrhage of, 609 

heruiae of, 609 

hydrometra, 607 

hypergemia of, 609 

hyperplasia, adenomatous, of, 612 

hyperplasia, glandular, of, 611 

infantile, characters of, 35 

inflammation, infectious, of, 615 

inflammation of (see Metritis and 
Endometritis) , 611 

inflammation, s^yphilitic, of, 614 

inflammation, tuberculous, of, 613 

lesions of. ref. Iloen, 487 

malformation of, 606 

Qvula Nabothi of, 612 

perforations of, 609 

perimetritis, 615 

phlebitis of, 616 

polypi of, 617 

pregnant, lesions of, 615 

prolapse of, 608 

rudimentar3% 607 
'-^ rupture of, 609 

size, shape, and situation of, 35 

syphilis of, 614 

tuberculosis of, 613 

tumors of, 616 

ulcers of, 610 

version of, 608 

weight of, 35 

Vaccination in smallpox, 249 
Vacuoles in cells, 84 
Vacuoles in renal epithelium, 580 
Vacuolization in cells, 84 
Vagina, absence of, 604 

bacteria of, 606 

bacteria of, ref. Williams, 611 

closure of, 604 
52 



Vagina, cysts of, 606 

dilatation of, 604 

double, 604 

examination, post-mortem, of, 35 

gangrene of, 606 

herniae of, 604 

inflammation of (see Vaginitis), 605 

inflammation, tuberculous, of, 606 

lengthening of, 604 

malformations of, 604 

narrowing of, 604 

parasites of, 606 

perforation of, 605 

prolapse of, 604 

rectal fistulae of, 605 

tumors of, 606 

vesical fistulae of, 605 

wounds of, 605 
Vaginitis, catarrhal, 605 

croupous, 605 

diphtheritic, 605 

membranous, 605 

suppurative, 606 

syphilitic, 606 

tuberculous, 606 
Van Gehuchten, Nervous System, ref. 730 
Van Gieson, ref. artefacts of the nervous 
system, 17, 715 

on death from electricity, 48 

on false heterotopia of spinal cord, 717 

on method of hardening spinal cord, J 9 

on Meynert's method of opening the 
brain, 15 

on toxic basis of neural diseases, 335 
Van Gieson' 8 stain (picro-acid fuchsin), 60, 
Varices, oesophageal, 550 
Variola, 249 

immunity in, 172 
Varix, aneurismal, 419 
Vaughan on ptomain poisoning, ref. 328 
Vaiiglian and JVory on ptomainsand leuco- 

mains, ref. 161, 328 
Vegetations, endocardial, 406 
Vein, portal, embolism of, 538 

portal, examination of, at autopsj^, 
32 

portal, dilatation of. 538 

portal, inflammation of, 538 

portal, lesions of, 537 

portal, rupture of, 538 

portal, thrombosis of, 537 

stones, 73 
Veins, 422 

anastomosing, 422 

calcification of, 423 

degeneration, fatty, of, 423 

dilatation of, 422 

hepatic, lesions of, 538 

iutlammation of (see Phlebitis), 423 

mesenteric, thrombosis of, 506 

parasites of, 425 

perforations of. 423 

rupture of, 423 

thrombosis of, 423 

tumors of, 425 

varicose, 422 

Avounds of, 423 



818 



INDEX. 



Vena cava, thrombosis of, 423 

Venom of scorpions and snakes, 162, 327 

Ventricles of brain, lesions of, 711 

of brain, parasites of, 714 
Veratria, poisonous effects of, 325 
Vernix caseosa, period of appearance of, 

in fa>tiis, 40 
VesiculcE seminales, post-mortem examina- 
tion of, 34 
Vessels, hepatic, lesions of, 537 
Vibrio Massawah, 217 

Metschnikovi, 217 

proteus, 217 
Vierordt, Anatomical Tables, 8 
Vircliow's work on tumors, ref. 319 
yogel on accessory lung, ref. 443 
D. Heukelom on experimental cirrhosis, ref. 

551 
Von Hibler on the gonococcus, ref. 194 
V. KaMden, ref. on multiple aneurism, 416 

on ovarian cysts, 637 
-y. Klecki on elimination of bacteria by the 

kidneys, ref. 577 
V. Lingelsheim, ref. on staphylococcus py- 
ogenes aureus, 183 

on streptococcus, 185 
Yon JSoorden, ref. on chlorosis, 355 

on diabetes, 334 
-y, Scheiber on tonsils as portals of entry for 

tubercle bacilli, ref. 488 
■y. Volkmann on endothelioma, ref. 295, 529 
Vulva, condyloma of, 603 

congestion, hypersemia of, 602 

cysts of, 604 

elephantiasis of, 603 

examination, post-mortem, of, 35 

gangrene of, 603 

haemorrhage of, 602 

hypergemia of, 602 

inflammation of (see Vulvitis), 602 

inflammation, syphilitic, of, 603 

inflammation, tuberculous, of, 603 

malformations of, 602 

mucous patch of, 603 

noma of, 603 

tuberculosis of, 602 

tumors of, 603 

varicose veins of, 602 
Vulvitis, 602 

syphilitic, 603 

tuberculous, 603 

WadsicortJi on puerperal infections, ref. 616 
Walsh on the excitant of whooping-cough, 

ref. 251 
Warrington on nerve cells, ref. 737 
Warthin, ref. on accessory adrenals, 385 

on pancreatitis, 532 

on parenchyma-cell emboli, 75 

on tumors and calculi of gall ducts, 
562 
Warts, 280 
Waschkewitsch on diphtheritic lesions of 

lymph-nodes, ref. 236 
Water, bacteria in, 147 
Waxy degeneration, 82 

degeneration, iodine test of, 28 



Wechsberg on early stages of tubercles, ref. 

219 
Weigert, ref. on excitants of cell growth, 
273 
on tumors of pineal gland, 768 
Weigerfs hgematoxylin method for stain- 
ing nerve tissue, 769 
modification of Gram's stain, 151 
Weight and size of organs, tables of, ref. 

Vierordt, 8 
Weil's disease, 539 
Weir on duodenal ulcers, ref. 508 
Weiss on bacteria in stomach of cat, ref. 

497 
Welch, ref. on air embolism, 354 

on adaptation in pathological proc- 
esses, 395 
on bacillus aerogenes capsulatus, 244 
on bacterial flora of body, 159 
on capsules of bacteria, method of 

staining, 192 
on carcinoma of stomach, 502 
on cirrhosis hepatis anthracotica, 551 
on oedema of lung, 445 
on pulmonary embolism, 446 
on thrombosis, 73, 75, 423, 506 
on ulcer of stomach statistics, 498 
Wentworth on typhoid meningitis, ref. 211 
Whipham, ref. on carcinoma, primary, of 
the appendix, 520 
on mediastinitis, ref, 481 
Whipworm, 136 

White blood cells, emigration of, 70 
White, ref. on bacteria in septicsemic 
blood, 181 
on staphylococcus pyogenes aureus in 
skin disease, 183 
Whooping-cough, 251 
Wiclimann on amyloid degeneration, ref. 

83 
WidaVs reaction, 213 
Wiener on sarcoma of intestine, ref. 519 
Williams, ref. on bacteria of vagina and 
uterus, 611 
on deciduoma, 626 
on placental infarcts, 627 
on sarcoma, primary, of pericardium, 
390 
Williams, H. V., on summary of plasma 

cells, ref. 103 
Wilms, ref. on teratomata of ovary, 637 

on teratoma of testicle, 657 
Wilson, The Cell in Development and In- 
heritance, ref. 98, 272 
Winkler on myeloma, ref. 681 
Wood naphtha in Delafield's hjematoxylin, 

59 
Woodman and Tidy on poisons, ref. 328 
Wool-sorters' disease, 198 
Wormley on poisons, ref. 328 
Worms, 130, 134 

earth-, regeneration in, 99 
methods of study of, 138 
Wounds, changes in, preceding repair, 117 
healing of, 99, 117 
of arteries, 410 
of heart, 393 



INDEX. 



819 



Wounds of pericardium, 387 

of spleen, 372 

post-mortem appearances of, 8 
Wright, ref. on Madura foot, 201 

on myeloma, 681 
Wriglit, J., on nasal polyps, ref. 429 
Writer's cramp, 739 

Xerosis bacillus, 239 

Yeasts, 140, 156, 158 
Yellow fever, 248 



Yersin, anti-plague serum of, 243 
Young on gonococcal infection, ref. 192 

Zahn on ciliated cysts, ref. 278 

on ciliated cysts of pleura, ref. 437 
Zenker's fluid for fixation, formula and 

uses of, 54 
Ziegler, ref. Text-book of Pathological An- 
atomy, 319 
on tumors, 273 
Zielil's solution, formula for, 223 
Zoogloea, 142 



D 



3/9^6 
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